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Natural Ways to Fix a Leaky Blood-Brain Barrier in Functional Neurology Part 2

Natural Ways to Fix a Leaky Blood-Brain Barrier in Functional Neurology Part 2

The blood-brain barrier is a protective shield that allows nutrients to enter the brain while keeping harmful components in the bloodstream from passing into the brain. However, many factors can cause a leaky blood-brain barrier. This can allow harmful components to penetrate the blood-brain brain, ultimately causing inflammation and brain health issues. A leaky blood-brain barrier is associated with many mental health issues and neurological diseases, including anxiety, depression, brain fog, fatigue, Alzheimer’s disease, Parkinson’s disease, attention deficit hyperactivity disorder (ADHD), and schizophrenia. In the article below, we will discuss natural ways which have been demonstrated to help fix a leaky blood-brain barrier and improve overall brain health.  

Take Berberine

A variety of plants have an alkaloid known as berberine. This extracted substance has anti-inflammatory properties and it can ultimately promote brain health by protecting neurons. Scientists have also found that taking berberine can help lower “bad” cholesterol, improve gut health, and many others believe it may even have possible antidepressant properties. Other research studies have shown that it can reduce inflammation, improve blood-brain barrier permeability and decrease damage following a traumatic brain injury. However, further research studies are still required to demonstrate these effects.  

Avoid Exposure to Mold

Mold and mycotoxins, or toxic metabolites released by mold, can cause severe brain health issues in people with certain sensitivities and intolerances. Exposure to these can also cause a leaky blood-brain barrier. In 2010, scientists demonstrated that exposure to mold and mycotoxins can increase BBB permeability by breaking down the blood-brain barrier. Moreover, low amounts of mold and mycotoxins can also be found in the foods we eat, including nuts, tea, coffee, and chocolate. Charcoal or bentonite clay supplements are powerful remedies that can capture toxins and release them out of the body.  

Take B Vitamins

According to healthcare professionals, B vitamins have been found to help improve a leaky blood-brain barrier. B vitamin deficiencies can ultimately affect brain health. Taking vitamin B1 (thiamine) supplements can help fix BBB permeability. Research studies have also shown that vitamins B6, B9, and B12 can help improve brain health in older adults with increased homocysteine and moderate cognitive impairment. Homocysteine is an inflammatory component that can breakdown the blood-brain barrier. Fortunately, healthcare professionals have found that taking B vitamins can balance the blood-brain barrier.  

Take Magnesium

Magnesium is a fundamental mineral that plays a vital role in a variety of structures and functions in the body, including enzyme, hormonal, and neurotransmitter activity. Magnesium is also one of the nutrients that people are most deficient in. This important mineral can increase growth hormones in the brain, support mitochondria, protect the brain from alcohol and help people overcome addiction and withdrawal. Research studies have also shown that taking magnesium can improve BBB permeability. Bananas, avocado, spinach, chard, almonds, pumpkin seeds, and dark chocolate have magnesium.  

Take R-Lipoic Acid (RLA) and Acetyl-Carnitine (ALCAR)

R-Lipoic Acid (RLA) is a fat-soluble and stable, bioavailable form of lipoic acid or an antioxidant created by the body, that can pass through the blood-brain barrier and enter the brain. This essential antioxidant can also protect the brain from alcohol and support mitochondria. Research studies have found that RLA can decrease oxidative stress and inflammation as well as improve BBB permeability and. Acetyl-Carnitine (ALCAR) is an acetylated form of the amino acid carnitine that is synergistic with RLA. ALCAR is neuroprotective and it can help people improve brain fog as well as addiction and withdrawal.  

Eat or Take Turmeric or Curcumin

Turmeric or curcumin, the spice that gives curry its yellowish color, is another fundamental ingredient for brain health that can help reduce stress and increase growth hormones in the brain. Turmeric or curcumin can also improve BBB permeability and promote overall brain health by maintaining and regulating the integrity of the blood-brain barrier. Research studies have also found that eating or taking turmeric or curcumin can help prevent damage to the blood-brain barrier due to glucose and oxygen deprivation by considerably decreasing oxidative stress and inflammation in the brain and body.  

Take Vitamin D

Vitamin D is another fat-soluble vitamin that the skin produces when exposed to the sun. The brain, heart, muscles, and immune system, among other cells and tissues in the body, have vitamin D receptors. This fat-soluble vitamin is fundamental for a variety of structures and functions. Vitamin D deficiencies can also cause a variety of brain health issues and neurological diseases. Scientists have shown that vitamin D can decrease inflammation and improve BBB permeability. Vitamin D has also been demonstrated to help protect endothelial cells and improve BBB permeability in patients with multiple sclerosis.  

Take Citicoline or Alpha GPC

Citicoline or CDP-Choline is another essential B vitamin and bioavailable form of choline. This substance can help improve brain fog. Research studies have also found that citicoline or CDP-Choline can prevent the breakdown of the blood-brain barrier following a stroke or traumatic brain injury and brain ischemia. Alpha GPC is another form of choline that has been shown to help support the blood-brain barrier. Scientists have also found that it can fix damage to the blood-brain barrier following a stroke or TBI, restoring cognitive function. You can also find some choline in egg yolks and beef liver.  

Avoid Exposure to EMFs

According to a variety of research studies, radiofrequency electromagnetic fields or EMFs emitted from smartphones, laptops, and WiFi can affect the brain and mental health. Radiofrequency electromagnetic fields or EMFs can cause a leaky blood-brain barrier.��Several other research studies have found that radiofrequency electromagnetic fields or EMFs can increase BBB permeability. Increased blood-brain barrier permeability may ultimately result in the accumulation of brain cell and tissue damage as well as cognitive impairment. It’s important to be aware of the effects of being exposed to these devices.   Dr. Alex Jimenez Insights Image
Many factors can cause a leaky blood-brain barrier, ultimately causing increased BBB permeability, oxidative stress, inflammation and a variety of brain and mental health issues, including neurodegenerative diseases. The blood-brain barrier is a protective shield which allows nutrients to enter the brain while keeping harmful components in the bloodstream from passing into the brain. A leaky blood-brain barrier is associated with anxiety, depression, brain fog, fatigue, Alzheimer’s disease, Parkinson’s disease, attention deficit hyperactivity disorder (ADHD), and schizophrenia. Fortunately, several natural ways have been demonstrated to help improve overall brain health and wellness as well as help fix a leaky blood-brain barrier. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
  The blood-brain barrier is a protective shield that allows nutrients to enter the brain while keeping harmful components in the bloodstream from passing into the brain. However, many factors can cause a leaky blood-brain barrier. This can allow harmful components to penetrate the blood-brain brain, ultimately causing inflammation and brain health issues. A leaky blood-brain barrier is associated with many mental health issues and neurological diseases, including anxiety, depression, brain fog, fatigue, Alzheimer’s disease, Parkinson’s disease, attention deficit hyperactivity disorder (ADHD), and schizophrenia. In the article above, we discussed more natural ways which have been demonstrated to help fix a leaky blood-brain barrier and improve overall brain health.  

The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.�

  Curated by Dr. Alex Jimenez   References:
  • The Star Academy. �How to Repair a Leaky Blood-Brain Barrier.� The Star Academy, The Star Academy, 16 Oct. 2018, thestaracademy.co.za/repair-leaky-blood-brain-barrier/.
 
 

Neurotransmitter Assessment Form

[wp-embedder-pack width=”100%” height=”1050px” download=”all” download-text=”” attachment_id=”52657″ /]   The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. The following symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue.  
 

Additional Topic Discussion: Chronic Pain

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.    
 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor   Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention.  

Food Sensitivity for the IgG & IgA Immune Response

Food Sensitivity Zoomer | El Paso, TX Chiropractor   Dr. Alex Jimenez utilizes a series of tests to help evaluate health issues associated with food sensitivities. The Food Sensitivity ZoomerTM is an array of 180 commonly consumed food antigens that offers very specific antibody-to-antigen recognition. This panel measures an individual�s IgG and IgA sensitivity to food antigens. Being able to test IgA antibodies provides additional information to foods that may be causing mucosal damage. Additionally, this test is ideal for patients who might be suffering from delayed reactions to certain foods. Utilizing an antibody-based food sensitivity test can help prioritize the necessary foods to eliminate and create a customized diet plan around the patient�s specific needs.  

Gut Zoomer for Small Intestinal Bacterial Overgrowth (SIBO)

Gut Zoomer | El Paso, TX Chiropractor   Dr. Alex Jimenez utilizes a series of tests to help evaluate gut health associated with small intestinal bacterial overgrowth (SIBO). The Vibrant Gut ZoomerTM offers a report that includes dietary recommendations and other natural supplementation like prebiotics, probiotics, and polyphenols. The gut microbiome is mainly found in the large intestine and it has more than 1000 species of bacteria that play a fundamental role in the human body, from shaping the immune system and affecting the metabolism of nutrients to strengthening the intestinal mucosal barrier (gut-barrier). It is essential to understand how the number of bacteria that symbiotically live in the human gastrointestinal (GI) tract influences gut health because imbalances in the gut microbiome may ultimately lead to gastrointestinal (GI) tract symptoms, skin conditions, autoimmune disorders, immune system imbalances, and multiple inflammatory disorders.  
Dunwoody Labs: Comprehensive Stool with Parasitology | El Paso, TX Chiropractor
GI-MAP: GI Microbial Assay Plus | El Paso, TX Chiropractor
 

Formulas for Methylation Support

Xymogen Formulas - El Paso, TX

  XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900. xymogen el paso, tx For your convenience and review of the XYMOGEN products please review the following link. *XYMOGEN-Catalog-Download   * All of the above XYMOGEN policies remain strictly in force.  
   
 

Modern Integrated Medicine

Natural Ways to Fix a Leaky Blood-Brain Barrier in Functional Neurology Part 1

Natural Ways to Fix a Leaky Blood-Brain Barrier in Functional Neurology Part 1

The blood-brain barrier is a protective shield that allows nutrients to enter the brain while keeping harmful components in the bloodstream from passing into the brain. However, many factors can cause a leaky blood-brain barrier. This can allow harmful components to penetrate the blood-brain brain, ultimately causing inflammation and brain health issues. A leaky blood-brain barrier is associated with many mental health issues and neurological diseases, including anxiety, depression, brain fog, fatigue, Alzheimer’s disease, Parkinson’s disease, attention deficit hyperactivity disorder (ADHD), and schizophrenia. In the article below, we will discuss natural ways which have been demonstrated to help fix a leaky blood-brain barrier and improve overall brain health.  

Improve Gut Health

Understanding the connection between the brain and the gut is important to treat a leaky blood-brain barrier. In 2014, scientists found that a group of mice that didn’t have bacteria in their gastrointestinal tract had very leaky blood-brain barriers. However, when the scientists of the research study introduced bacteria into the intestines of the unhealthy mice through a fecal transfer, their BBB permeability considerably improved. Increasing good bacteria in your gut can ultimately help improve a leaky blood-brain barrier. Eating probiotics, prebiotic fiber, and fermented foods can increase good bacteria in your GI tract.  

Avoid Eating Gluten

According to many healthcare professionals, we should avoid eating gluten to promote brain health. In 2006, scientists found that gluten can cause a leaky blood-brain barrier because it increases zonulin, a protein that affects BBB permeability and results in neuroinflammation. Gluten sensitivity or intolerance can also cause visible changes in the white matter of the brain. Dr. David Perlmutter, MD, author of Grain Brain and Brain Maker states that gliadin, another protein found in gluten, can also affect BBB permeability. Moreover, other food sensitivities or intolerances can also cause a leaky blood-brain barrier.  

Eat Food with Sulforaphane

Cruciferous vegetables, including Brussels sprouts, cabbage, and broccoli, among others, have sulforaphane, a phytochemical and well-known antioxidant with powerful anti-inflammatory properties, similar to turmeric or curcumin. Many research studies have shown that sulforaphane can help improve a leaky blood-brain barrier by decreasing BBB permeability, preventing the breakdown of the BBB, and improving cognitive functions after stroke and traumatic brain injuries. Sulforaphane in myrosinase-activated supplement form can also be taken. Myrosinase is an enzyme in broccoli that helps metabolize sulforaphane.  

Eat Food with Resveratrol or Pterostilbene

Foods like raspberries, grapes, red wine, and dark chocolate have resveratrol, another powerful antioxidant with potent anti-inflammatory properties that can help prevent the development of neurodegenerative diseases caused by a leaky blood-brain barrier. Scientists have found that eating food with resveratrol can ultimately help promote growth hormones in the brain and support mitochondria function. According to research studies, resveratrol can also protect the blood-brain barrier. Numerous other research studies have also found that eating foods with resveratrol can have other health benefits, including:  
  • Decreasing a leaky blood-brain barrier
  • Protecting the blood-brain barrier
  • Improving blood-brain barrier permeability
  Research studies have also shown that resveratrol can help protect the blood-brain barrier against oxidized LDL-induced damage. Furthermore, scientists believe that eating food with resveratrol may be a safe and effective way to naturally reduce the severity of multiple sclerosis.�Foods like blueberries have pterostilbene, a substance similar to resveratrol, that can also help protect the blood-brain barrier by decreasing oxidative stress and inflammation. Many healthcare professionals also refer to pterostilbene as the “better resveratrol” because it is often believed to be best absorbed by the body than resveratrol.  

Drink More Coffee

Caffeine can help promote overall brain health and support the blood-brain barrier. Research studies have shown that drinking coffee can help prevent the development of dementia, Alzheimer’s disease, and Parkinson’s disease, among other health issues, by protecting the BBB. Scientists have also found that caffeine blocks blood-brain barrier permeability. Other research studies have also shown that drinking coffee can help prevent neurodegeneration by balancing the BBB. Because drinking coffee and caffeine can commonly affect sleep, however, make sure to consume these early in the morning.  

Take Omega-3 Fatty Acids

Omega-3 fatty acids are essential fats that are primarily found in fish. Although the body can’t produce these by itself, they are necessary for overall brain health. Omega-3 fatty acids can also help increase the growth hormones in the brain, help support mitochondria function, or help people overcome addiction and withdrawal, as well as help protect the blood-brain barrier. Scientists have found that taking omega-3 fatty acids can decrease damage to the BBB following a stroke or TBI and improve BBB permeability in people with multiple sclerosis. Omega-3 fatty acids can also be taken in supplement form.  

Take Melatonin and Improve Sleep

Sleep is fundamental for brain health. Poor sleep has also been shown to increase blood-brain barrier permeability. Taking melatonin supplements can also help improve sleep.�Melatonin is a hormone that is released by a small gland in the brain, known as the pineal gland. Melatonin helps regulate the circadian rhythm, or sleep and wake cycles. Enough melatonin is necessary to fall asleep quickly and sleep deeply throughout the night. Research studies have also shown that taking melatonin can help balance the blood-brain barrier and prevent further damage following a stroke and/or traumatic brain injury.  

Manage and Reduce Stress

According to research studies, stress can ultimately damage the blood-brain barrier. Chronic stress has also been found to increase inflammation and BBB permeability. Fortunately, managing and reducing stress can help fix the blood-brain barrier. Massage, acupuncture, eye movement desensitization and reprocessing (EMDR), emotional freedom techniques (EFT), heart-rate variability (HRV) training, and mindfulness meditation can also help manage and reduce stress. Taking supplements to help improve stress can also include, zinc, magnesium, ashwagandha, and phosphatidylserine, among others.  

Avoid Drinking Alcohol

According to healthcare professionals, drinking too much alcohol can cause a leaky blood-brain barrier. Research studies have shown that acetaldehyde, a byproduct of alcohol metabolism, can increase oxidative stress and affect the blood-brain barrier, resulting in inflammation and a variety of neurological diseases and brain health issues. Although some types of alcohol are better than others, it’s best to considerably decrease or avoid drinking alcohol. If you suspect that you may have a leaky blood-brain barrier, make sure to talk to your doctor about how drinking too much alcohol may cause a leaky BBB.   Dr. Alex Jimenez Insights Image
Many factors can cause a leaky blood-brain barrier, ultimately causing increased BBB permeability, oxidative stress, inflammation and a variety of brain and mental health issues, including neurodegenerative diseases. The blood-brain barrier is a protective shield which allows nutrients to enter the brain while keeping harmful components in the bloodstream from passing into the brain. A leaky blood-brain barrier is associated with anxiety, depression, brain fog, fatigue, Alzheimer’s disease, Parkinson’s disease, attention deficit hyperactivity disorder (ADHD), and schizophrenia. Fortunately, several natural ways have been demonstrated to help improve overall brain health and wellness as well as help fix a leaky blood-brain barrier. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
  The blood-brain barrier is a protective shield that allows nutrients to enter the brain while keeping harmful components in the bloodstream from passing into the brain. However, many factors can cause a leaky blood-brain barrier. This can allow harmful components to penetrate the blood-brain brain, ultimately causing inflammation and brain health issues. A leaky blood-brain barrier is associated with many mental health issues and neurological diseases, including anxiety, depression, brain fog, fatigue, Alzheimer’s disease, Parkinson’s disease, attention deficit hyperactivity disorder (ADHD), and schizophrenia. In the next article, we will discuss more natural ways which have been demonstrated to help fix a leaky blood-brain barrier and improve overall brain health.  

The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.�

  Curated by Dr. Alex Jimenez   References:
  • The Star Academy. �How to Repair a Leaky Blood-Brain Barrier.� The Star Academy, The Star Academy, 16 Oct. 2018, thestaracademy.co.za/repair-leaky-blood-brain-barrier/.
 
 

Neurotransmitter Assessment Form

[wp-embedder-pack width=”100%” height=”1050px” download=”all” download-text=”” attachment_id=”52657″ /]   The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. The following symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue.  
 

Additional Topic Discussion: Chronic Pain

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.    
 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention.  

Food Sensitivity for the IgG & IgA Immune Response

Food Sensitivity Zoomer | El Paso, TX Chiropractor Dr. Alex Jimenez utilizes a series of tests to help evaluate health issues associated with food sensitivities. The Food Sensitivity ZoomerTM is an array of 180 commonly consumed food antigens that offers very specific antibody-to-antigen recognition. This panel measures an individual�s IgG and IgA sensitivity to food antigens. Being able to test IgA antibodies provides additional information to foods that may be causing mucosal damage. Additionally, this test is ideal for patients who might be suffering from delayed reactions to certain foods. Utilizing an antibody-based food sensitivity test can help prioritize the necessary foods to eliminate and create a customized diet plan around the patient�s specific needs.  

Gut Zoomer for Small Intestinal Bacterial Overgrowth (SIBO)

Gut Zoomer | El Paso, TX Chiropractor Dr. Alex Jimenez utilizes a series of tests to help evaluate gut health associated with small intestinal bacterial overgrowth (SIBO). The Vibrant Gut ZoomerTM offers a report that includes dietary recommendations and other natural supplementation like prebiotics, probiotics, and polyphenols. The gut microbiome is mainly found in the large intestine and it has more than 1000 species of bacteria that play a fundamental role in the human body, from shaping the immune system and affecting the metabolism of nutrients to strengthening the intestinal mucosal barrier (gut-barrier). It is essential to understand how the number of bacteria that symbiotically live in the human gastrointestinal (GI) tract influences gut health because imbalances in the gut microbiome may ultimately lead to gastrointestinal (GI) tract symptoms, skin conditions, autoimmune disorders, immune system imbalances, and multiple inflammatory disorders.  
Dunwoody Labs: Comprehensive Stool with Parasitology | El Paso, TX Chiropractor
GI-MAP: GI Microbial Assay Plus | El Paso, TX Chiropractor
 

Formulas for Methylation Support

Xymogen Formulas - El Paso, TX

  XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900. xymogen el paso, tx   For your convenience and review of the XYMOGEN products please review the following link. *XYMOGEN-Catalog-Download   * All of the above XYMOGEN policies remain strictly in force.  
 
Functional Neurology: What is the Role of the Blood-Brain Barrier?

Functional Neurology: What is the Role of the Blood-Brain Barrier?

Our brain is a complex organ protected by our 7mm thick skull, a protective membrane, known as the meninges, and cerebrospinal fluid. These essential brain structures help protect the brain against physical damage or injury. Another brain structure that protects the brain from harm is the blood-brain barrier. The blood-brain barrier is the shield between the brain’s blood vessels and the cells in the brain’s tissue. While the skull, meninges, and cerebrospinal fluid protect the brain from physical damage or injury, the blood-brain barrier protects the brain from toxins and pathogens in the bloodstream. �

 

Moreover, the presence of the blood-brain barrier in the human brain was first discovered in the late 1800s by the German scientist Paul Ehrlich when he injected blue dye in the bloodstream of a group of mice during an experiment. The blue dye strained all of the animals’ tissues and organs with the exception of the brain and spinal cord. Although the outcome measures of the research study demonstrated the existence of the blood-brain barrier, it wasn’t until the 1960s that researchers were able to use much more powerful technologies to ultimately prove the presence of the blood-brain barrier in the human brain. �

 

Anatomy of the Blood-Brain Barrier

The main structure of the blood-brain barrier that helps protect the brain from toxins and pathogens in the bloodstream is known as the endothelial tight junction. The endothelial cells cover the inside of the blood vessels in the brain. The blood-brain barrier is such an effective security system because these endothelial cells in the blood vessels in the brain are connected extremely close to each other in “tight junctions”. The blood-brain barrier only permits small, fat-soluble molecules and several types of gases to pass freely between the blood vessels and the brain. Furthermore, bigger molecules, such as glucose and insulin, are only permitted passage through transporter proteins which act like “bouncers” that only open the doors for certain necessary molecules. �

 

The purpose of the blood-brain barrier is to protect the brain against toxins and pathogens circulating in the bloodstream that could cause brain health issues while also permitting passage to fundamental nutrients that are necessary for the brain. Other functions of the blood-brain barrier include regulating and managing consistent levels of nutrients, hormones, and water in the human brain. Changes in these may affect the homeostasis of the brain. �

 

The homeostasis of the brain can commonly be affected by bacterial infections, such as meningococcal disease. Meningococcal bacteria can attach to the endothelial cells of the blood vessels in the brain and cause the tight junctions to slightly open. This causes the blood-brain barrier to become more porous which can then permit passage to toxins and pathogens that can infect the brain tissue, leading to inflammation and sometimes even death. It�s also believed that the blood-brain barrier can decrease in a variety of other brain health issues. In multiple sclerosis, by way of instance, decreased blood-brain barrier function may permit white blood cells to pass into the brain and attack the structures that transmit messages from one neuron to another. �

 

Blood-Brain Barrier Treatment

The blood-brain barrier is so effective at protecting the brain from toxins and pathogens that it can even block necessary treatments from reaching the brain. The vast majority of potential drugs and/or medications that could help treat a variety of brain health issues aren’t able to readily penetrate the blood-brain barrier which may become a tremendous problem in treating neurological diseases. However, one possible way to penetrate the blood-brain barrier is to �trick� the security system into permitting passage to certain medicines. The blood-brain barrier can also be temporarily opened using ultrasound. �

 

One research study demonstrated that using ultrasound to temporarily open the blood-brain barrier in a mouse with Alzheimer�s disease can improve cognition and decrease toxic plaques in the brain. But most importantly, using ultrasound to temporarily open the blood-brain barrier didn�t damage or injure the brain. In another research study, researchers demonstrated that by temporarily opening the blood-brain barrier, ultrasound can permit the passage of drugs and/or medications into the brain, improving cognition and Alzheimer’s disease more than when using ultrasound or medicines alone. �

 

Dr. Alex Jimenez Insights Image

After the discoveries of the German scientist Paul Ehrlich during the late 1800s, a collection of experiments on a group of mice demonstrated how the brain regulates what to permit passage to and what to block from entering its blood vessels through the blood-brain barrier. The brain is ultimately protected by the blood-brain barrier, however, this security system can frequently prevent drugs and/or medications from being able to effectively treat brain health issues. Scientists have started working towards developing successful ways to allow treatments to penetrate the blood-brain barrier. Other research studies have demonstrated that by using ultrasound, the blood-brain barrier can be temporarily opened to permit passage for medicines to help treat a variety of brain health issues and neurological diseases, among other problems.�- Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Neurotransmitter Assessment Form

Neurotransmitter Assessment Form AE260 (1)

 

The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. The following symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �

 


 

Our brain is a complex organ that is protected by our 7mm thick skull, a protective membrane, known as the meninges, and cerebrospinal fluid. These essential brain structures ultimately help protect the brain against physical damage or injury. Another brain structure that protects the brain from harm is the blood-brain barrier. The blood-brain barrier is the shield between the brain’s blood vessels and the cells in the brain’s tissue. While the skull, meninges, and cerebrospinal fluid protect the brain from physical damage or injury, the blood-brain barrier protects the brain from toxins and pathogens in the bloodstream. �

 

Moreover, the presence of the blood-brain barrier in the human brain was first discovered in the late 1800s by the German scientist Paul Ehrlich when he injected blue dye in the bloodstream of a group of mice during an experiment. The blue dye strained all of the animals’ tissues and organs with the exception of the brain and spinal cord. Although the outcome measures of the research study demonstrated the existence of the blood-brain barrier, it wasn’t until the 1960s that researchers were able to use much more powerful technologies to ultimately prove the presence of the blood-brain barrier in the human brain. �

 

The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.�

 

Curated by Dr. Alex Jimenez �

 

References:

  • Woodruff, Alan. �What Is the Blood-Brain Barrier?� Queensland Brain Institute, 11 Jan. 2018, qbi.uq.edu.au/brain/brain-anatomy/what-blood-brain-barrier.

 


 

Additional Topic Discussion: Chronic Pain

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance. �

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

 

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Food Sensitivity for the IgG & IgA Immune Response

Food Sensitivity Zoomer | El Paso, TX Chiropractor

 

Dr. Alex Jimenez utilizes a series of tests to help evaluate health issues associated with food sensitivities. The Food Sensitivity ZoomerTM is an array of 180 commonly consumed food antigens that offers very specific antibody-to-antigen recognition. This panel measures an individual�s IgG and IgA sensitivity to food antigens. Being able to test IgA antibodies provides additional information to foods that may be causing mucosal damage. Additionally, this test is ideal for patients who might be suffering from delayed reactions to certain foods. Utilizing an antibody-based food sensitivity test can help prioritize the necessary foods to eliminate and create a customized diet plan around the patient�s specific needs. �

 

Gut Zoomer for Small Intestinal Bacterial Overgrowth (SIBO)

Gut Zoomer | El Paso, TX Chiropractor

 

Dr. Alex Jimenez utilizes a series of tests to help evaluate gut health associated with small intestinal bacterial overgrowth (SIBO). The Vibrant Gut ZoomerTM offers a report that includes dietary recommendations and other natural supplementation like prebiotics, probiotics, and polyphenols. The gut microbiome is mainly found in the large intestine and it has more than 1000 species of bacteria that play a fundamental role in the human body, from shaping the immune system and affecting the metabolism of nutrients to strengthening the intestinal mucosal barrier (gut-barrier). It is essential to understand how the number of bacteria that symbiotically live in the human gastrointestinal (GI) tract influences gut health because imbalances in the gut microbiome may ultimately lead to gastrointestinal (GI) tract symptoms, skin conditions, autoimmune disorders, immune system imbalances, and multiple inflammatory disorders. �

 


Dunwoody Labs: Comprehensive Stool with Parasitology | El Paso, TX Chiropractor


GI-MAP: GI Microbial Assay Plus | El Paso, TX Chiropractor


 

Formulas for Methylation Support

Xymogen Formulas - El Paso, TX

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

Please call our office in order for us to assign a doctor consultation for immediate access.

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

For your convenience and review of the XYMOGEN products please review the following link. *XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Functional Neurology: Nrf2 Activation for Neurological Diseases

Functional Neurology: Nrf2 Activation for Neurological Diseases

Neurological diseases, including well-known neurodegenerative disorders like Alzheimer’s disease (AD) and Parkinson’s disease (PD) as well as other rare health issues, such as Huntington’s disease (HD) and amyotrophic lateral sclerosis (ALS), affect millions of people worldwide. Unfortunately, these are estimated to increase due to the aging population. Currently, there is no treatment available for any neurodegenerative disorder. Treatments for symptoms are available for several neurological diseases, such as PD and HD, but the therapeutic benefits are limited. Although the causes and symptoms for these health issues are different for each neurodegenerative disorders, their molecular pathogeneses share common underlying factors and characteristics, including excessive levels of reactive oxygen species (ROS), mainly due to mitochondrial impairment, neuroinflammation, and disturbances in protein homeostasis (proteostasis). This increases the possibility of developing a universal treatment that will focus on targeting the common triggers of neurological diseases. �

 

Nrf2 Activation Pathways and the Human Brain

The transcription factor, Nrf2, regulates the main endogenous defense mechanism against oxidative and xenobiotic stress and inflammation. Nrf2 also plays a fundamental role in the management of mitochondrial function and cellular proteostasis, which suggests the possible benefits of Nrf2 to control neurodegenerative disorders. When under stress, Nrf2 activates the transcriptional upregulation of a large network of cytoprotective genes that allow adaptation and survival. The levels and activity of Nrf2 are controlled through ubiquitination and proteasomal degradation mediated by several ubiquitin ligase systems, including Keap1-Cul3/Rbx1, ?-TrCP-Cul1, and Hrd1. Keap1 is the most well understood key regulator of Nrf2. �

 

Keap1 functions as a primary sensor for electrophiles and oxidants, which chemically change certain cysteines in Keap1, leading to conformational changes that protect Nrf2 from Keap1-associated degradation. Subsequently, Nrf2 will accumulate and then translocate to the nucleus where it binds as a heterodimer with a small Maf transcription factor to antioxidant response elements in the promoter of its target genes to activate the expression of a large network of detoxification, antioxidant, and anti-inflammatory genes as well as other genes involved in the clearance of damaged proteins. Of particular interest is also the upregulation of genes responsible in the biosynthesis and the regeneration of glutathione (GSH), a major intracellular antioxidant. Moreover, Nrf2 also suppresses proinflammatory responses through transcriptional repression and it is involved in the regulation of mitochondrial function. Keap1 and p62/SQSTM1 are Nrf2-associated proteins and main regulators of negative and positive feedback loop mechanisms. In addition, p62 targets Keap1 for selective degradation through autophagy, therefore contributing to the sustained Nrf2 activation response. �

 

Aging has been associated with the increase in ROS and chronic inflammation, which suggests a loss of adaptability and/or impairment of Nrf2 signaling, which are particularly pronounced in age-dependent neurodegenerative disorders. Surprisingly, rare mutations in SQSTM1 can cause susceptibility to the human neurodegenerative disorder, ALS as well as frontotemporal lobar degeneration, and are associated with muted Nrf2 activation responses in clinical trials. Research studies suggest a reciprocal correlation and show negative effects of mutant disease-related proteins on Nrf2 signaling, thus suggesting the inhibition of the Nrf2 pathway as a possible mechanism underlying neurodegeneration and health issues. �

 

Nrf2 Activation for Neurodegenerative Disorders

ALS, an adult-onset neurodegenerative disorder caused by the selective death of motor neurons in the brain and spinal cord, is commonly characterized by progressive muscle weakness and atrophy which is generally considered to be fatal, typically within 5 years of diagnosis. ALS has a predominant sporadic ALS form with no apparent genetic component, however, approximately 5 to 10 percent of cases show an autosomal dominant inheritance pattern or familial form of the disease, known as fALS, with is known to cause gene mutations. The symptoms of sporadic ALS and familial ALS are similar, which suggests the involvement of common pathogenic mechanisms, including oxidative stress and neuroinflammation. �

 

Research studies show that oxidative stress and neuroinflammation should be the key therapeutic targets of Nrf2 signaling in ALS. Genetic research studies in ALS mouse models have shown a considerable therapeutic effect of increased Nrf2 levels in astrocytes, the main GSH producers for neurons. Furthermore, Nrf2 signaling is fundamental for controlling neuroinflammation in ALS through the management of the effects of activated microglial cells on overall neuronal survival. Consistent with the therapeutic potential of Nrf2 signaling, treatment with small molecule activators, including the extremely potent cyanoenone triterpenoids, has ultimately shown efficacy in research study mouse ALS models. �

 

The neuroprotective potential of Nrf2 activation has been evaluated in experiments utilizing genetic mouse HD models. HD is an autosomal dominant and highly penetrant neurodegenerative disorder, which results from the pathological expansion of a trinucleotide CAG repeats encoding polyglutamines in HTT protein. Brains from patients with HD usually show marked striatal and cortical atrophy at the time of diagnosis. Once motor or other symptoms become apparent, generally throughout midlife, the affected individuals become increasingly disabled over the course of 15 to 25 years before eventually succumbing to the effects of severe physical and mental deterioration, according to evidence from research studies. �

 

Complex pathogenic mechanisms have been shown in HD, however, excessive oxidative stress has been recognized as a fundamental driver of pathology. The harmful role of oxidative stress has been described in both HD patients and in experimental clinical trial models and it is potentially due to the neuronal sensitivity of an excess in ROS. The levels of several Nrf2-dependent antioxidant proteins, including glutathione peroxidases, catalase, and superoxide dismutase 1, are increased in human HD brains as compared with non-disease controls, suggesting a partial activation of Nrf2 defense signaling yet insufficient enough to block progressive neurodegeneration. Pharmacological activation of Nrf2 results in the broad antioxidant effects of HD in mouse brains and ameliorates the neurological phenotype. Increased expression of several key inflammatory mediators has been shown in the blood, the striatum, the cortex, and the cerebellum from postmortem patient HD tissues, however, neuroinflammation in HD patients seems to be less pronounced than in ALS or PD patients. �

 

Neurological Disease Treatment with Nrf2 Activation

Finally, the neurological phenotype of the most common neurological disease and neurodegenerative disorder, PD, can be challenged by Nrf2 activation. PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra and the profound reduction of dopamine in the striatum. Currently available dopaminergic treatments offer relief from several symptoms but these only address the motor manifestations. Multiple genetic and environmental factors have been suggested in the etiology of PD, however, like ALS, the majority of the clinical cases are sporadic. The discovery that the environmental neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes Parkinson’s disease in humans, led to the development of the MPTP mouse model of disease, which to date, remains one of the most highly utilized animal models of sporadic PD, including the evaluation of drug efficiency. Nrf2 activators showed neuroprotective effects in MPTP mice, which are associated with a reduction of oxidative damage and neuroinflammation. The identification of causative mutations in SNCA, the gene encoding ?-synuclein (aSyn), developed genetic mouse PD models, in which daily oral delivery of the Nrf2 activator dimethyl fumarate (DMF) protected nigral dopaminergic neurons against aSyn toxicity. �

 

Although oxidative stress and neuroinflammation are pathological hallmarks of AD, a therapeutic role of Nrf2 signaling has developed more slowly, perhaps due to the complexity of disease pathogenesis and readouts of efficiency. Nonetheless, there is a number of recent research studies that demonstrate the efficiency of Nrf2 activators in AD mouse models. � DMF, a U.S. FDA-approved drug (Tecfidera, Biogen-Idec) for the treatment of relapsing multiple sclerosis, activates Nrf2 through the regulation of the Keap1 sensor. DMF is of seemingly low potency and specificity, which prevents neurodegeneration. Drug-like molecules with a similar mechanism of action or with the ability of direct interference with the Keap1/Nrf2 interaction are emerging. The data demonstrate the feasibility to develop Nrf2 activators for treatment. �

 

El Paso Chiropractor Staff and Doctor

In summary, although the causes and symptoms of neurological diseases are different, neurodegenerative disorders share similar molecular mechanisms, which could be regulated and managed with Nrf2 activators. Moreover, targeting Nrf2 signaling may offer a safe and effective treatment approach for a variety of these health issues. Because pharmacological Nrf2 activation targets the broad mechanisms of these health issues, all neurodegenerative conditions would be eligible for treatment. Furthermore, the main goal is to develop noninvasive oral treatment(s) for patients under the supervision of healthcare professionals, which targets both sporadic and familial patients. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Neurotransmitter Assessment Form

Neurotransmitter Assessment Form AE260 (1)

 

The following Neurotransmitter Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptoms listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �

 


 

Neurological diseases, including well-known neurodegenerative disorders like Alzheimer’s disease (AD) and Parkinson’s disease (PD) as well as other rare health issues, such as Huntington’s disease (HD) and amyotrophic lateral sclerosis (ALS), affect millions of people worldwide. Unfortunately, these are estimated to increase due to the aging population. Currently, there is no treatment available for any neurodegenerative disorder. Treatments for symptoms are available for several neurological diseases, such as PD and HD, but the therapeutic benefits are limited. Although the causes and symptoms for these health issues are different for each neurodegenerative disorders, their molecular pathogeneses share common underlying factors and characteristics, including excessive levels of reactive oxygen species (ROS), mainly due to mitochondrial impairment, neuroinflammation, and disturbances in protein homeostasis (proteostasis). This increases the possibility of developing a universal treatment that will focus on targeting the common triggers of neurological diseases. �

 

The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 

References:

 

  • Dinkova-Kostova, Albena T, et al. �Activation of Nrf2 Signaling as a Common Treatment of Neurodegenerative Diseases.� Activation of Nrf2 Signaling as a Common Treatment of Neurodegenerative Diseases | Neurodegenerative Disease Management, 23 May 2017, www.futuremedicine.com/doi/full/10.2217/nmt-2017-0011#.

 


 

Additional Topic Discussion: Chronic Pain

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Food Sensitivity for the IgG & IgA Immune Response

Food Sensitivity Zoomer | El Paso, TX Chiropractor

Dr. Alex Jimenez utilizes a series of tests to help evaluate health issues associated with food sensitivities. The Food Sensitivity ZoomerTM is an array of 180 commonly consumed food antigens that offers very specific antibody-to-antigen recognition. This panel measures an individual�s IgG and IgA sensitivity to food antigens. Being able to test IgA antibodies provides additional information to foods that may be causing mucosal damage. Additionally, this test is ideal for patients who might be suffering from delayed reactions to certain foods. Utilizing an antibody-based food sensitivity test can help prioritize the necessary foods to eliminate and create a customized diet plan around the patient�s specific needs. �

 

Formulas for Methylation Support

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link. *XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Functional Neurology: MSG and Neurological Diseases

Functional Neurology: MSG and Neurological Diseases

MSG is a food additive which is found in the majority of the industrial foods. It boosts the taste of the food hence attracting customers. There is no value in terms of nutrition and it really does nothing to the eater, however, it can have many effects on foods. MSG is known as an “excitotoxin” or neurotoxin. Research studies have found that it has devastating and degenerative effects on the brain and the nervous system. The neurons or brain cells overstimulate and fatigue to their death. MSG enters the brain through the membranes in the mouth and the throat. It also enters the blood-stream through the digestion of food in the gastrointestinal (GI) tract. MSG “tricks” the human body into believing that it is getting value from these foods. �

 

MSG is not a natural substance found in nature. It’s a man-made chemical from glutamic acid, an amino acid found in proteins. Amino acids do happen naturally in animal cells and in several plant cells. The kinds of amino acids have been processed through the change of this pure form of glutamate. Some of the materials used for this purpose include starches, molasses, and corn. The manipulation procedure generates this type of glutamate. The d-glutamate is not found naturally. The free glutamates can enter the body about eight to ten times faster compared to natural glutamates. Natural glutamate is found in foods such as tomatoes, mushrooms, and milk. Techniques used to manufacture glutamate were not in use before the 1960s. The MSG in use now is not natural. In the article, we will discuss how MSG is associated with neurological diseases. �

 

Research Studies on MSG and Neurological Diseases

 

Research studies indicate that MSG is the reason for neurological diseases like Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and Amyotrophic lateral sclerosis. Neuroscientists have explained that MSG attacks the blood-brain barrier of the neurons which is responsible for the regulation of the fragile chemical exchange inside the brain cells. The chemical exchange process is well balanced and its performance is unquestionable. Under normal conditions, the brain and the entire immune system manage all sorts of toxins, health issues, and stress. A very small amount of poisonous substances can actually make the brain overreact, ultimately resulting in excessive exhaustion and death, according to research studies. �

 

MSG is a leading “excitotoxin” and it is widely known to cause harm to the brain region which governs or controls additional systems from the human body. The damage will seem like a disease in the endocrine system and the immune system. This can be shown in the cases of food cravings, persistent hunger, and unusual sleeping patterns. This normally leads to obesity. MSG is also known to cause migraine headaches, behavioral disorders, depression, asthma attacks, heart problems, arthritis, sinus issues, and digestive issues. �

 

MSG is a neurotoxin which requires an extremely brief time to create a broadly diverse and dramatic effect on the human body. An individual may have a mild dose of a prescription drug and also have favorable effects. However, another individual might take the prescription drug and get sad, have a swollen tongue, stomach disorders, and joint problems. The different parts of the brain affected do govern various body functions. The part which is attacked will depend on the individual. If by way of instance, an individual has had a headache, a genetic pinch in a given portion of the brain, has had a fever that’s attacking regions of the brain, or has had a stroke, then it’s certain that the component of the brain that has been affected will be due to the toxins. �

 

A number of the foods sold are ultimately sold as weight loss promotions to the people. MSG, along with aspartame, is added when food substances, such as fat and sugar, are eliminated from the meals. These excitotoxins have been known to cause obesity and irregular heartbeats. FDA generally allows the labeling of MSG’S as natural flavors, hydrolyzed proteins, and autolyzed yeast, when used as just a partial ingredient in an additive rather than only MSG. Americans now are consuming 160 million lbs of MSG per year. Author and toxicologist Dr, George Schwartz asserts that two tablespoons of MSG on bread could kill a medium-sized dog within a moment. The FDA in 1995 claimed that no one can respond to less than 3 grams of MSG per meal. In spite of their confirmation, they’ve warned that children, pregnant or lactating women, and the elderly should avoid MSG. An extremely sensitive individual can also ultimately react even to under a gram of MSG. �

 

Effects of MSG and Neurological Diseases

 

Research studies have shown that from the late 1950s, an estimated amount of 12 grams per person of MSG was utilized by most Americans each year. These days, taking a look at precisely the same health issue, the quote is between 400 and 500 g per person each year. This is an amount which requires evaluation. The wide usage of MSG arrived in the mid-1970s. It gained much popularity throughout the 1980s with manufacturers of food. Two powerful excitotoxic food additives which took the food sector by storm have been the use of MSG and aspartame. MSG has been broadly associated with a wide assortment of symptoms and health issues. As previously stated, it affects the human body’s neurological system. The same ailments are being reported to be on their rise. The ailments are absolutely unexpected and difficult to describe. �

 

Neurological diseases associated with MSG and numbers of interest released by federal organizations have been recorded in fibromyalgia, which is a growing epidemic. Its patients eliminated aspartame and MSG during the research study conducted by the Florida University which reported complete relief of symptoms. On the other hand, the most cognitive research study was conducted to prove the connection between fibromyalgia and MSG along with several different additives as a common rheumatologic disorder. In this case, 4 patients had been diagnosed for 2 to 17 years with fibromyalgia syndrome. They had undergone various methods of therapy whilst failing to consider MSG as the causative agent. After eliminating aspartame and MSG in their diets, complete or near complete resolution of symptoms diagnosed was listed within months. The subjects were women who had recurring symptoms and multiple comorbidities. It’s therefore indicative that the excitotoxins, present in compounds, such as aspartate and MSG, become excitatory neurotransmitters once ingested and when consumed in excess may lead to neurotoxicity. These 4 patients may, therefore, signify this fibromyalgia syndrome and act as a link to conclusively establish a link to MSG. Therefore, persistent research studies, if carried out on a larger sample, might serve to connect the fibromyalgia syndrome into MSG and aspartame more concretely. Further research studies are required. �

 

Moreover, a research study connected MSG to adrenal adenomas. The hypothalamus which leads damage on the nerves is overstimulated by MSG. The hypothalamus is responsible for directing the pituitary gland’s actions, which can be known as the endocrine gland since it in turn directs the rest of the glands in the human body and their activities such as metabolism, development of reproductive and sex organs and other essential development functions. Statistics have demonstrated that 25 percent of Kenyans have a pituitary adenoma. However, research studies linking pituitary adenomas to MSG have ultimately been inconclusive. Some research studies had depicted this as a disease but have been proven wrong. �

 

About half of the pituitary adenomas secrete prolactin. These can become large over time in the optic nerve, thus, affecting vision. It also prevents ovulation and menses. This prevents pregnancy or conception generally. Furthermore, since prolactin is responsible for lactation, lactation can be caused by secretion in the individual even if they’re male or even when they were not pregnant. Men with these adenomas grow breasts. Since the tumor can only be discovered when it’s big and dangerous unlike in women that are forewarned by the effects on vision or related headaches, this problem is deadly in men. There’s a further need to sponsor more research studies so as to ultimately associate MSG and brain tumors, among others. �

 

Other effects which were attributed to MSG and neurological diseases are headaches and migraines, asthma, and obesity amongst others. In headaches and migraines, an approximate amount of $2.2 billion each year are being spent on drugs and/or medicines that treat head pain. This chronic condition has received a 74 percent increase. Second, asthma associated with the brain was connected to MSG. According to data, there was a decrease of asthma before the mid-eighties. Since then, however, there’s been a 100 percent gain in the rate of death among children and seniors. This prevalence has increased by 600 percent in the last 10 years. FDA has identified that uncontrollable asthma can be caused by MSG, sadly, no measures are taken to take care of the situation. In defects of birth and disorders of production, MSG was identified as a mutagen i.e. mutates fetuses. It’s reputed to cause damage to the development, reproduction, and growth patterns as well as the functions. Such research studies have not been concrete. Other consequences include emotional or neurological disorders. Laboratory research studies demonstrate devastating effects on brain development, including dyslexia, attention deficit, autism, hyperactivity, violent episodes or rage, panic attacks, depression, paranoia, seizures and cerebral palsy. Rats were utilized with this research study. However, human beings are five times more sensitive to MSG than rats. �

 

This topic of ailments in behavior for children is becoming a frequent discussion amongst professionals. These have associated attention deficits, behaviour, and instability to chemical imbalances occurring in the brain. It is now becoming an intense possibility that there’ll be damage caused by excitotoxins in the blood-brain barrier of young brains. �

 

In April 1994, a magazine article confirmed the rising problem of behavioral disorders. The magazine stated that the attention deficit hyperactivity disorder wasn’t in existence. It’s however said that it is currently affecting 3.3 million American kids. This magazine article estimates prominent research studies which 10 years ago stated that symptoms of ADHD and ADD vanished with maturity. Nowadays, however, ADD is the fastest growing diagnostic category for adults. The combination of both excitotoxins i.e. MSG and aspartame came into wide utilization in the 1980s. �

 

El Paso Chiropractor Dr. Alex Jimenez

In the medical field, a controversy as to whether MSG is associated with neurological diseases has been determined. Monosodium glutamate, or MSG, has been utilized as a flavorant in the food industry for approximately 100 years and it is consumed by the masses on a regular basis today. Although the FDA, or the Food and Drug Administration, categorizes MSG as a safe food ingredient, many research studies have determined that it can cause a variety of health issues, including neurodegenerative diseases, among others. – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Metabolic Assessment Form

Metabolic Assessment Form AE266

 

The following Metabolic Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptom groups listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue. �

 


 

In honor of Governor Abbott’s proclamation, October is Chiropractic Health Month. Learn more about the proposal. � MSG is a food additive. It boosts the taste of food, attracting customers. There is no nutrition and it really does nothing to the eater, however, it can have many effects on foods. MSG is known as an “excitotoxin” or neurotoxin. Research studies have found that it has devastating and degenerative effects on the brain and the nervous system. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Microglial Priming in Alzheimer’s Disease

Microglial Priming in Alzheimer’s Disease

Alzheimer�s disease (AD) is one of the most common types of dementia among older adults. Research studies have demonstrated that pathological changes in the human brain, whether directly or indirectly, can ultimately cause loss of synaptic function, mitochondrial damage, microglial cell activation, and neuronal cell death. However, the pathogenesis of AD is not yet fully understood and there is currently no definitive treatment for the neurological disease. Research studies have demonstrated that the activation and priming of microglial cells may contribute to the pathogenesis of AD. �

 

A proinflammatory status of the central nervous system (CNS) can also cause changes in the function of the microglial cells or microglia. Neuroinflammation is closely associated with the activation of microglia and astrocytes which are connected to a variety of neurological diseases by the synthesis and secretion of inflammatory mediators such as iNOS, ROS, and proinflammatory cytokines. According to research studies, microglial priming is also caused by the inflammation of the CNS. �

 

Therefore, whether microglial priming is the result or the cause of neuroinflammation is still controversial. Microglial cell activation commonly causes an increase of A? and tau proteins as well as a decrease of neurotrophic factors, ultimately leading to the loss of healthy brain cells or neurons and the development of neuritic plaques and neurofibrillary tangles which are closely associated with AD. With the progression of Alzheimer’s disease, changes from neuronal dysfunctions which may have no obvious symptoms to memory loss and cognitive impairment may become more noticeable. �

 

Microglial Priming, Neuroinflammation, and AD

 

Although the accurate and detailed, fundamental role of the microglial cells continues to be discovered and explained, there is a consensus among many researchers that primed microglia are associated with the inflammatory response of the CNS in AD. It has also been determined that neuroinflammation caused by microglial priming is mainly associated with aging, systemic inflammation, gene regulation, and blood-brain barrier impairment. The purpose of the article below is to discuss how microglial priming and neuroinflammation in Alzheimer’s disease can be caused due to a variety of risk factors. �

 

Aging

 

Aging is considered to be one of the main risk factors for AD and it is generally followed by chronic, systemic up-regulation of pro-inflammatory factors and a considerable decrease in an anti-inflammatory response. This change from homeostasis to an inflammatory state occurs through age-related elements which cause an imbalance between anti-inflammatory and pro-inflammatory systems. Microglia is primed into an activated state which can increase the consistent neuroinflammation and inflammatory reactivity in the aged human brain. Research studies have demonstrated that microglia in the brain of rodents developed an activated phenotype during aging characterized by the increased expression of CD11b, CD11c, and CD68. �

 

Systemic Inflammation

 

Recent research studies have determined that the neuroinflammation from primed microglial cells can also cause the pathogenesis of AD. Continuous activation of microglia can promote the synthesis and secretion of pro-inflammatory cytokines and trigger a pro-inflammatory response, ultimately causing neuronal damage. Neuroinflammation is an early symptom in the progression of AD. The microglia can have a tremendous effect on the inflammation of the human brain. �

 

The inflammation and health issues of the CNS can be associated with systemic inflammation through molecular pathways. One research study demonstrated that ROS development of primed microglia decreases the levels of intracellular glutathione and increases nitric oxide in NADPH oxidase subunit NOX2. Moreover, researchers demonstrated that these simultaneously occurring processes ultimately cause the development of more neurotoxic peroxynitrite. This is demonstrated in rodents with peripheral LPS or proinflammatory cytokines, such as TNF-?, IL-1?, and IL-6, IL-33. �

 

The outcome measures of numerous research studies have demonstrated that systemic inflammation can cause microglial activation. The results of the research studies emphasize the variability of the inflammatory response in the human brain associated with AD and the underlying health issues associated with systemic inflammation and neuroinflammation, as shown in Table 1. MAPK (mitogen-activated protein kinase) signaling pathways regulate mechanisms of the eukaryotic cell and microglial MAPK can also cause an inflammatory response to the aged brain with AD. Furthermore, chronic or continuous systemic inflammation causes neuroinflammation, resulting in the onset and accelerating the progression of AD. �

 

Table 1 Effects of Inflammatory Cytokines in AD | El Paso, TX Chiropractor

Genetic Regulation

 

In the aging human brain, gene regulation has ultimately been associated with an innate immune response. Recent preclinical, bioinformatics, and genetic data have demonstrated that the activation of the brain immune system is associated with the pathology of AD and causes the pathogenesis of this neurological disease. Genome-wide association studies (GWAS), functional genomics, and even proteomic evaluations of cerebrospinal fluid (CSF) and blood have demonstrated that dysfunctional immune pathways from genic mutation are risk factors in LOAD, which is the vast majority of AD. �

 

GWAS have become a fundamental tool in the screening of genes as well as demonstrating several new risk genes associated with AD. Apolipoprotein E (APOE) ?4allele is one of the most considerable and well-known risk genes for sporadic AD and this mutation ultimately increases the risk of neurological disease onset by 15 times in homozygous carriers and by three times in heterozygous carriers. Further research studies have demonstrated how microglial cell function can be affected through a variety of rare mutations which have demonstrated to have an increased risk factor of Alzheimer’s disease. �

 

An extracellular domain mutation of the TREM2 gene has also demonstrated an almost identical extent with APOE?4 in increasing the risk factor of AD. TREM2 is increasingly demonstrated on the surface of microglia and mediates phagocytosis as well as the removal of neuronal debris. Additionally, several other genes, such as PICALM, Bin1, CLU, CR1, MS4A, and CD33 have been demonstrated as risk genes for AD. Most of the risk mutation genes are expressed by microglial cells. �

 

Blood-Brain Barrier (BBB) Impairment

 

The blood-brain barrier (BBB) is a specialized barrier commonly developed between the blood and the brain by tight liner sheets consisting of specific endothelial cells and tight junctions or structures which connects a variety of cells together. The CNS is fundamental for the human body, and the BBB is fundamental for the CNS. The BBB and the blood-nerve barrier develop a defense system to control the communications of cells and soluble factors between blood and neural tissue where it plays a considerable role in maintaining and regulating the homeostasis of the CNS and peripheral nervous system. �

 

With development, continuous inflammation can also cause damage to the BBB. This damage can ultimately cause loss of hypersensitive neurons, neuroinflammatory regions, and focal white matter impairment following the damage. The compromised BBB also allows more leukocytes to enter into the CNS where an immune response can be aggravated by brain microglia under the condition of peripheral inflammation. These processes may ultimately be under the control of chemokine and cytokine signaling which can also have an effect on brain microglial cells as well as other health issues in AD. �

 

By way of instance, it has been determined that TNF-?, IL-17A, and IL-1? can reduce the tight junctions and eliminate the BBB. Loss of BBB integrity and abnormal expression of tight junctions are associated with neuroinflammation. Several research studies also demonstrated in an animal model of AD that the vulnerability of BBB to inflammation increases. Current evidence has also demonstrated that the BBB integrity is fundamental while further evidence of the BBB may demonstrate a new treatment approach for AD associated with microglial priming as shown in Figure 2 below. �

 

Microglial Priming and AD | El Paso, TX Chiropractor

Conclusion

 

Microglia play a fundamental role in maintaining and regulating the homeostasis of the CNS’s micro-environment. If the balance of the homeostasis of the human brain is interrupted, the microglial cells can be activated to restore the balance in the CNS by defending against the stimulation and protecting the structure and function of the brain. However, chronic and continuous stimulation can trigger microglia into a state known as microglial priming, which is more sensitive to potentially minor stimulation, causing a variety of health issues, such as central sensitization, chronic pain, and fibromyalgia. �

 

Microglial priming mainly causes the boost of A?, tau protein as well as neuroinflammation and reduces neurotrophic factors which can cause the loss of healthy brain cells or neurons as well as the development of neuritic plaques and neurofibrillary tangles which are associated with Alzheimer’s disease. Although this �double-edged sword� plays a fundamental role, it can increase the progression of abnormal protein development and aggravate neuronal loss and dysfunction. However, research studies have ultimately demonstrated that aging can cause the progression of AD and there’s not much we can do about it. �

 

El Paso Chiropractor Dr. Alex Jimenez

Microglial cells play a fundamental role as the protectors of the brain and they ultimately help maintain as well as regulate the homeostasis of the CNS microenvironment. However, continuous stimulation can cause the microglia to trigger and activate at a much stronger state which is known as microglial priming. Once the microglial cells go into protective mode, however, primed microglia can become much more sensitive to even minor stimulation and they have a much stronger possibility of reacting towards normal cells. Microglial priming has been associated with neuroinflammation and Alzheimer’s disease (AD) as well as central sensitization and fibromyalgia. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

AD is one of the most common types of dementia among older adults. However, the pathogenesis of AD is misunderstood and there is no definitive treatment for the neurological disease. Research studies have ultimately demonstrated that the activation and priming of microglial cells may contribute to the pathogenesis of AD. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

 

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Microglial Priming in the Central Nervous System

Microglial Priming in the Central Nervous System

Microglial cells make up about 10 to 15 percent of all the glial cells in the human body, which can be found in the central nervous system (CNS) and play a fundamental role in the human brain. Microglial cells are responsible for maintaining and regulating changes in the physiological and pathological condition of the CNS by changing their morphology, phenotype and function. In an average physiological state, the microglial cells are continuously in charge of controlling their environment. �

 

However, when the homeostasis of the brain is interrupted, the microglia change into an amoeba-like shape and become a phagocyte where they can actively reveal a variety of antigens. If the homeostasis interruption in the CNS continues, the microglial cells will then trigger at a much stronger state, which is known as microglial priming. Microglia are the “Bruce Banner” of the CNS. However, once they go into protective “Hulk” mode, primed microglia become much more sensitive to stimulation and they have a much stronger possibility of reacting to stimulation, even reacting towards normal cells. �

 

Microglial Cells are Bruce Banner and Hulk in CNS | El Paso, TX Chiropractor

 

Microglial priming can become a double-edged sword. As a matter of fact, primed microglia are created from different phenotypes of microglia and the phenotypes are context-dependent, which means they are associated to the sequence and duration of their exposure to different varieties of stimulation in a variety of pathologies. In the article below, we will demonstrate the effect of microglial priming on the central nervous system (CNS), especially in neurological diseases. �

 

Role of Microglial Cells in the CNS

 

Microglial cells are commonly found in the central nervous system (CNS), where they are considered to be one of the most flexible types of brain cells. Microglial cells are created from precursor cells found within mesoderm bone marrow, or more specifically found in the mesodermal yolk sac, and they are divided in different densities throughout several regions of the brain. As mentioned above, microglia will remain in a dormant state when the homeostasis of the brain remains stable. �

 

Microglia have a small cell body and morphological branches which extend towards all directions to help maintain and regulate the overall function of the CNS. Changes in their microenvironment can trigger microglia into an “activated� state. Research studies have demonstrated that microglia play a fundamental role in brain development and a variety of functions, including synaptic pruning and clearing out cell debris. Moreover, microglia create an immune surveillance system in the human brain and control fundamental processes associated with a variety of pathologies, including the clearance and uptake of A? and abnormal tau protein as well as the production of neurotrophic factors and neuroinflammatory factors. �

 

Microglial Priming Overview

 

Microglial priming activates when continuous interruptions in the brain’s microenvironment trigger a much stronger microglial response compared to an initial interruption which simply triggers microglial activation. Primed microglia in the CNS are also much more sensitive to possibly minor stimulation. This increased response involves microglial proliferation, morphology, physiology, and biochemical markers or phenotype. However, these changes will ultimately promote an increase in cytokines and inflammation mediator production which can have a tremendous impact on synaptic plasticity, neuronic survival, individual cognitive and behavioral function. Below is an overview of the effects of microglial priming in the CNS. �

 

Mechanisms of Microglial Priming in the CNS

 

The microenvironment of the central nervous system (CNS), by way of instance, is one of the main factors which can affect the microglial cells. Increased oxidative stress, lipid peroxidation and DNA damage associated with brain aging can all commonly trigger microglial priming. Another common factor for microglial priming includes traumatic brain injury. Research studies have shown that traumatic CNS injury activates microglia as well as the development of primed microglia. �

 

Many research studies have also shown that both focal and diffuse traumatic brain injury increase inflammation in the brain associated with microglia and astrocytes. CNS infections can also trigger microglial priming where viruses are the main cause of CNS infection. Both DNA and RNA viruses can trigger microglial priming including microglia and astrocytes. Recent research studies have shown that complement dysfunction can change the expression of complement receptors and trigger microglial priming after continuous activation following a variety of functions, including synapse maturation, immune product clearance, hematopoietic stem/progenitor cells (HSPC) mobilization, lipid metabolism, and tissue regeneration. �

 

Moreover, research studies have shown that there is increased priming of the microglia in a variety of neurological diseases. By way of instance, microglial cells with a morphological phenotype are found in large numbers in the human brain. In the last several years, research studies have suggested that neuroinflammation can continuously activate the microglia and trigger microglial priming. Furthermore, all of the previously mentioned situations are closely associated with neuroinflammation. Research studies have also demonstrated that neuroinflammation, as well as microbial debris and metabolic effects, are associated with central sensitization in neurological diseases, such as fibromyalgia, also referred to as the “brain on fire”. �

 

In the context of the previous situations mentioned above, microglia are primed though a series of pro-inflammatory stimulation, such as lipopolysaccharide (LPS), pathogenetic proteins (e.g., A?), ?synuclein, human immunodeficiency virus (HIV)-Tat, mutant huntingtin, mutant superoxide dismutase 1 and chromogranin A. There is also a variety of signaling pathways and it is common for different types of cells to express special pattern recognition receptors (PRRs) which can affect inflammatory signaling pathways. By way of instance, several signaling pathways, known as pathogen-associated molecular patterns (PAMPs), which can commonly increase in infected tissue, could also control microbial molecules. �

 

Additionally, peptides or mislocalized nucleic acids identified as misfolded proteins through a series of pathways, known as danger-associated molecular patterns (DAMPs), can also cause microglial priming. Toll-like receptors (TLRs) and carbohydrate-binding receptors commonly function in these pathways. There are also many different receptors found in microglia, including triggering receptors expressed on myeloid cells (TREM), Fc? receptors (Fc?Rs), CD200 receptor (CD200R), receptor for advanced glycation end products (RAGE), chemokine receptors (CX3CR1, CCR2, CXCR4, CCR5, and CXCR3), which can be recognized and mixed in with other signaling pathways, although some pathways are still not clear. �

 

Consequences of Microglial Priming in the CNS

 

Microglia show a low rate of mitosis in their normal state and a high rate of proliferation after microglial priming, showing that the microglia have the ability to affect cell turnover and pro-inflammation stimulation. With continued stimulation, microglia activate from their resting state, changing into amoeboid microglial cells in morphology. However, the changes in the shape of the microglia cannot differentiate the characteristics of microglial activation and the function of primed microglia depends on their phenotypes which are associated with receptors and molecules which they create and recognize. �

 

The different types of tissue macrophages, under microenvironmental impetus, are able to differentiate M1 and M2 phenotypes. First, M1 polarization, also known as classical activation, ultimately needs interferon-? (IFN-?) to be mixed with TLR4 signaling which then causes the production of inducible nitric oxide synthases (iNOS), reactive oxygen species (ROS), proinflammatory cytokines, and finally, ultimately reduces the release of neurotrophic factors, ultimately causing inflammation with increased markers of main histocompatibility complex II (MHC II), interleukin-1? (IL-1?) and CD68. �

 

Moreover, M2 polarization, also known as alternative activation, is ultimately believed to be associated with tissue-supportive in the situation of wound healing, reducing inflammation and improving tissue repair of collagen form. They trigger in response to IL-4 and IL-13 in vivo. M2 polarization is characterized by the increased expression of neurotrophic factors, proteases, enzymes arginase 1 (ARG1), IL-10 transforming growth factor-? (TGF-?), scavenger receptor CD206 and coagulation factors as well as improving phagocytic activity. As a matter of fact, there are currently no clear boundaries between the two polarizations and the M1 phenotype shares many similar characteristics with the M2 phenotype. �

 

Another phenotype of primed microglia, known as acquired deactivation, has been recently discovered. This new phenotype overlaps with M2 and has the ability to improve anti-inflammatory and functional recovery. Additionally, a research study conducted ultra-structural analyses and identified a brand-new phenotype, known as �dark microglia�, which is rarely seen in the microglial cell’s resting state. Systemic inflammation triggers microglia into an activated state to promote cell and tissue recovery and achieve homeostasis. Microglial priming is ultimately the second interruption in the CNS microenvironment. �

 

The primed microglia is a double-edged sword for brain health. Many research studies in vivo and in vitro have shown that neurological diseases are associated with microglial activation. The inflammatory phenotypes of the microglia create neurotoxic factors, mediators and ROS which can affect the CNS. Primed microglia play a fundamental and beneficial role in neuronal regeneration, repair, and neurogenesis. Primed microglia are also much more sensitive and respond much stronger to brain injury, inflammation, and aging as well as increase the activation of microglial cells by switching from an anti-inflammation, potentially protective phenotype to a pro-inflammation destructive phenotype, as shown in (Figure 1). �

 

Figure 1 Microglial Priming and Altering | El Paso, TX Chiropractor

 

In the early stages of microglial priming, the ability and function to phagocytize cell debris, misfolded proteins, and inflammatory medium are increased where more protective molecules, such as IL-4, IL-13, IL-1RA, and scavenging receptors, are created. The changes can affect wound healing and damage tissue repairment, neuron protection, and homeostasis recovery. Classically activated microglia (M1) make up a large proportion of all microglia and promote an increased creation of neurotoxic factors, such as IL-1?, TNF-?, NO and H2O2 (6), where more microglia are primed immediately afterward. �

 

This increased and extended neuroinflammation caused by primed microglia can ultimately be associated with the development and clustering of the protein tau and A?. Furthermore, it can lead to loss of neurons as well as the decrease of cognitive function and memory, such as in Alzheimer’s disease. Although the mechanisms are not clear enough, people have reached an agreement that primed microglia cause a chronic proinflammatory response and a self-perpetuating cycle of neurotoxicity. And this is believed to be the key factor in brain health issues resulting in neurological diseases. �

 

Microglia are known as the protectors of the brain and they play a fundamental role in maintaining as well as regulating the homeostasis of the CNS microenvironment. Constant stimulation causes the microglia to trigger at a much stronger state, which is known as microglial priming. Microglial cells are the “Bruce Banner” of the CNS. However, once they go into protective “Hulk” mode, primed microglia become much more sensitive to stimulation and they have a much stronger possibility of reacting to stimulation, even reacting towards normal cells. �- Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

Microglial cells make up about 10 to 15 percent of all the glial cells in the human body, which can be found in the central nervous system (CNS) and play a fundamental role in the human brain. Microglial cells are responsible for maintaining and regulating changes in the physiological and pathological condition of the CNS. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

 

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Red Light Therapy for Neurological Diseases

Red Light Therapy for Neurological Diseases

About 6 million people in the United States have Alzheimer�s disease (AD) and about 50 million people worldwide have dementia. There aren’t many treatments to treat these neurological diseases. Scientists in a 2018 research study on red light therapy and mice described that �treatment for Alzheimer�s disease and dementia has not been effective for more than 100 years.� Another research study described that there is currently “no treatment to prevent brain health issues. �

 

However, research studies on red light therapy as a treatment for Alzheimer�s disease and dementia have been positive over the last few years in laboratory settings with rodent models. Based on this lab data, researchers recommend red light therapy and near-infrared light therapy in human patients with AD and dementia. In this article, we will look at what the initial human research studies on red light therapy and Alzheimer�s disease/dementia have shown over the last few years. �

 

Red Light Therapy for Alzheimer�s and Dementia

 

The first few double-blinded, placebo-controlled human trials on red light therapy for AD, dementia, and other neurological diseases published in 2017 had very positive results. The data showed that red light therapy caused changes in executive function, clock drawing, immediate recall, memory, visual attention, and task switching, among other positive results. One research study showed that patients treated with transcranial light therapy experienced improvements, such as: �

 

  • Increased cognitive function
  • Better sleep
  • Fewer angry outbursts
  • Less anxiety
  • Less wandering

 

The research study noted that there were �no negative side-effects� on transcranial light therapy for neurological diseases. The research study concluded that transcranial light therapy shows potential for the treatment of brain health issues. �

 

More Human Trials with Red Light Therapy in Progress

 

The results of these initial human trials are encouraging for Alzheimer’s disease and dementia patients and families looking for better treatment options, especially natural and non-invasive treatments with no drugs/medications or side effects. �

 

In early 2019, three more human trials on red light therapy and AD/dementia have been in progress at the University of California and a hospital system in France. With the previous positive results, more and larger research studies and human trials are being organized. Scientists hope that in the following years, the base of positive evidence will be large enough to recommend red light therapy as a treatment for Alzheimer�s disease and dementia, among other neurological diseases. �

 

The results from human trials over the last few years have established a much bigger base of similarly positive results from research studies of rodent brains in Alzheimer�s disease and dementia models, both of which are outlined below. �

 

Red Light Therapy Reduces Oxidative Stress and Improves Memory

 

A 2018 research study of mice in an age-related AD/dementia model showed that red light therapy considerably reduced oxidative stress levels and restored memory function. The researchers also praised red light therapy for being a non-invasive treatment option as well as having a high rate of tissue penetration and low phototoxicity. The researchers additionally found that red light therapy not only prevented early-stage memory decline but also recovered late-stage memory deficits. �

 

Researchers in a similar 2015 research study with a mouse AD/dementia model utilized near-infrared (NIR) light instead of red light therapy. The NIR treatments also reduced oxidative stress in the cerebellar cortex. The researchers concluded that NIR treatments had the ability to prevent brain degeneration in every region of the mouse brain. The research studies concluded that light therapy opens a promising opportunity to translate LED-therapy into treatments for patients. �

 

Red Light Therapy Prevents Brain Degeneration

 

Several research studies have shown that red light therapy can suppress the buildup of Beta-amyloid (A?), a protein which causes senile plaques in people with Alzheimer�s disease and dementia. Synaptic dysfunction, due to the disruptive binding of (A?) in the brain, is one of the symptoms of AD and dementia responsible for causing initial cognitive decline. Preventing synaptic dysfunction can be an effective treatment for AD and dementia, helping to regulate and manage symptoms. �

 

Red Light Therapy Improves Memory, Motor Skills, and Recognition

 

Research studies in 2017 evaluated the hippocampus of rat brains in an Alzheimer�s model with light therapy. Both research studies considerably reduced A? plaques in the rats treated with light therapy. Both research studies also tested the subjects and found that treatments reduced hippocampal neurodegeneration and improved spatial memory, recognition, and basic motor skills in the light therapy groups. Another research study also showed considerable A? reduction and noted that NIR light can reduce synaptic dysfunction from A?, showing that NIR light therapy is a viable treatment for AD and dementia. �

 

Red Light Therapy Shows Promise for Neurological Diseases

 

The initial research studies on red light therapy for Alzheimer�s disease and dementia have ultimately been encouraging for researchers. Red light therapy is not FDA-approved for the treatment of Alzheimer�s Disease or dementia, however, there is hope that more positive results in human trials will show that light therapy is fundamental for AD and dementia treatment. �

 

Based on the available base of positive evidence, however, red light therapy shows promise as a natural, non-invasive, drug/medication-free treatment for brain degeneration where pharmacological solutions have long failed. �

 

By reducing oxidative stress and preventing the accumulation of the Beta-amyloid which causes brain plaques and synapse dysfunction, red light therapy offers hope towards delaying the onset of Alzheimer�s disease and dementia symptoms as well as hopefully even reversing or preventing brain degeneration and cognitive function decline. Researchers, patients, and families affected by AD and dementia will be watching closely in the following years as more positive results emerge. �

 

Research studies have demonstrated positive results on red light therapy for Alzheimer’s disease and dementia. Initial research studies on mice and rat models have shown the effects of light therapy on neurological diseases. Although, more human trials are still necessary to establish the effectiveness of red light therapy for AD and dementia, the base positive results are promising. Many healthcare professionals can help treat the symptoms associated with a variety of neurological diseases, among other health issues. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

Research studies on red light therapy for AD and dementia have been positive over the last years. The initial human research studies on red light therapy and Alzheimer�s disease/dementia have been promising. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Diagnosis of Central Nervous System Infections Part 2

Diagnosis of Central Nervous System Infections Part 2

Central nervous system, or CNS, infections can be life-threatening if they are not diagnosed and treated early. Because CNS infections are non-specific, determining an accurate diagnosis can be challenging. The nucleic acid in vitro amplification-based molecular methods are starting to be utilized for routine microbial diagnosis. These molecular methods have improved beyond conventional diagnostic techniques with increased sensitivity and specificity. Moreover, molecular methods utilized on cerebrospinal fluid samples are considered the new standard for diagnosis of CNS infections caused by pathogens. �

 

Molecular methods for the diagnosis of CNS infections offers a variety of monoplex and multiplex PCR assays to diagnose several types of health issues. Pan-omic molecular platforms can also help diagnose CNS infections. Although molecular methods are utilized for the diagnosis of CNS infections, the outcome measures for these diagnostic techniques must be carefully identified by healthcare professionals. The following article discusses conventional diagnostic techniques and molecular methods utilized for the diagnosis of central nervous system infections, their application, and future approaches. �

 

Molecular Methods in the Diagnosis of CNS Infections

 

Because of increased sensitivity and specificity, nucleic acid in vitro amplification-based molecular methods has tremendously improved the ability to diagnose CNS infections in a reasonable and effective time frame. Several PCR-derived techniques have also ultimately increased the flexibility and rigor of currently available diagnostic techniques. �

 

Reverse transcriptase, or RT,-PCR was developed to increase RNA targets. Its utilization plays a fundamental role in the diagnosis of RNA-virus infections as well as managing their reaction to treatment. Timely access to enterovirus RT-PCR outcome measures has demonstrated shorter hospital stays, reduced unnecessary antibiotic utilization, and decreased ancillary laboratory evaluations and tests. Broad-range rRNA PCR techniques, which utilize a single pair of primers targeting conserved regions of genes, have been utilized to diagnose bacterial pathogens and herpes viruses in the CSF. Isothermal amplification-based techniques. including loop-mediated isothermal amplification or LAMP, have been developed to offer a diagnosis within several minutes to hours. Table 2 demonstrates commercial molecular in vitro diagnostic devices, or IVD, which have been cleared by the US Food and Drug Administration, or FDA, for diagnosis of microbial pathogens in CSF. �

 

Monoplex Assays

 

A conventional molecular method involves three phases: sample extraction, target nucleic acid amplification, and amplicon detection. One of the first molecular assays successfully utilized for the diagnosis of CNS infections was utilized for the diagnosis of HSV in cerebrospinal fluid or CSF. PCR became the test of choice when research studies demonstrated that CSF PCR was similar to culture of brain tissue for diagnosis of HSV encephalitis and meningitis. Many PCR based methods for the diagnosis of herpes and enteroviruses have become available with increased sensitivity compared to viral culture. �

 

Real-time PCR with nucleic acid amplification and amplicon detection further improved the transition to molecular methods in clinical laboratories. Unlike conventional PCR, the real-time system is a �closed� system and it overcomes the fundamental problem of carryover contamination. At the time of manuscript preparation, three molecular assays utilized to help diagnose HSV and enteroviruses in CSF have ultimately been approved by the FDA as demonstrated in Table 2 of the previous article. � Real-time PCR-based methods are the main diagnostic technique utilized to help diagnose the Zika virus, which was first reported in Uganda in 1947, and is now a worldwide concern after the virus spread widely in Brazil and Central America. Research studies developed a one-step RT-PCR assay utilized to diagnose the Zika virus in human serum with a limited detection of 7.7pfu/reaction. Along with plasma, the Zika virus RNA can be diagnosed through urine and plasma within the first 2 weeks after symptoms have manifested. In March 2016, the FDA approved a trioplex-PCR assay under emergency use authorization for the simultaneous diagnosis of Zika, Chikungunya, and Dengue viruses in serum, urine, CSF and amniotic fluid. The RT-PCR assay utilizes dual labeled hydrolysis probes with a LOD of 1.54�10 4 GCE/ ml of Zika virus in serum. �

 

Introduction of real-time PCR based diagnostic assays have affected early and effective diagnosis of several bacterial infections. Isothermal amplification-based molecular assays have excellent performance characteristics and they don’t require any specialized equipment. These assays are fundamental for the utilization of on or near point-of-care testing. LAMP-based methods have been utilized to diagnose Neisseria meningitis, Streptococcus pneumoniae, Haemophilus influenzae type b, M. tuberculosis, and JEV in the CSF. The Xpert MTB/RIF assay has tremendously improved regulation of tuberculosis by offering an integrated and automated system which allows quick clinical decision making in a POC or near-care context. Several research studies have utilized the Xpert MTB/RIF to evaluate the diagnosis of M. tuberculosis in CSF from TB meningitis. In a meta-analysis of thirteen research studies, the pooled sensitivity of the Xpert assay was 80.5 percent, or 95 percent CI 59.0 percent to 92.2 percent, against culture and 62.8 percent, or 95 percent CI 47.7 percent to 75.8 percent, against composite standard. Utilizing a large volume of sample, of at least 8�10 ml, is necessary for testing CSF and centrifugation can cause considerable improvements in yield. Despite the lack of standardization for sample processing, WHO has allowed testing CSF with the automated Xpert MTB/RIF assay as the first-line test over conventional microscopy. �

 

Multiplex Assays

 

Simplicity makes multiplex molecular assays fundamental for the diagnosis of a panel of microbial targets. Several multiplex PCR assays have been developed to diagnose bacterial pathogens in CSF targeting the most common causes of meningitis: S. pneumoniae, N. meningitis, H. influenzae, L. monocytogenes, S. agalactiae, S. aureus, E. coli, and M. pneumoniae. A multiplex PCR followed by Luminex suspension array can simultaneously diagnose eight bacterial and viral pathogens in CSF, including N. meningitis, S. pueumoniae, E. coli, S. aureus, L. monocytogenes, S. agalactiae, HSV-1/2, and VZV, among others. �

 

Considering the variety of pathogens involved in CNS infection, application of comprehensive molecular panels with multiple bacterial and viral targets have improved the efficiency of diagnosis. The BioFire FilmArray Meningitis/Encephalitis panel is currently the only FDA cleared multiplex assay utilized for the diagnosis of six bacterial, such as Escherichia coli K1, Haemophilus influenzae, Listeria monocytogenes, Neisseria meningitides, Streptococcus agalactiae and Streptococcus pneumoniae, seven viral, such as cytomegalovirus, enterovirus, HSV-1, HSV-2, human herpesvirus 6 or HHV-6, human parechovirus and VZV, as well as a single fungal, such as Cryptococcus neoformans/gattii, target in CSF as demonstrated in Table 2. The integrated FilmArray system takes about an hour, with only 2 minutes of hands-on time. During the preparation of the manuscript, two research studies demonstrated the performance of this assay. Utilizing 48 samples from gram stain negative CSF samples from suspected cases of meningitis, research studies demonstrated that this system diagnosed more viral pathogens, such as EBV. Four cases of WNV and a single case of Histoplasma were not diagnosed by this assay. Among HIV infected patients in Uganda, the test performance demonstrated increased sensitivity and specificity for the diagnosis of Cryptococcus. Although the FilmArray Meningitis/Encephalitis panel offers a quick diagnosis of CNS infections, further research studies are needed to determine its performance for a variety of targets and other high-risk populations. �

 

Co-infections are frequently found among immunocompromised patients and can ultimately be challenging to diagnose for clinicians. The multiplex design allows simultaneous diagnosis of multiple targets on the same sample. One research study utilized a panel of monoplex and multiplex molecular assays to conduct a prospective cohort research study in Uganda to comprehensively evaluate the etiology of meningitis among HIV-infected adults. Among the 314 HIV-infected patients with meningitis, EBV co-infection was diagnosed with Cryptococcus, M. tuberculosis, or other viral pathogens. EBV in CSF in these settings is not completely understood although a single research study associated increased EBV viral load as a marker of poor outcome measures in patients with bacterial meningitis and EBV co-infection/ reactivation, among others. �

 

Pan-Omic Molecular Assays

 

Technological improvements in metagenomic deep sequencing have increased its utilization for clinical diagnosis of CNS infections. Several research studies have demonstrated its ability to solve diagnostic technique problems which challenge the limits of traditional laboratory testing. Due to sterile status and protection by BBB, CSF and brain biopsies are fundamental to further explore the utilization of this technology for pathogen diagnosis. Metagenomics was successfully utilized to establish a diagnosis of neuroleptospirosis in a 14-year-old boy with severe combined immunodeficiency who also suffered from recurrent bouts of fever, headache, and coma. Similarly, high-throughput RNA sequencing performed on brain biopsy from an 18-month-old boy with encephalopathy diagnosed a new Astrovirus as the cause. Despite the utilization of metagenomics for the diagnosis of infectious disease, there are many technological and practical concerns which need to be addressed before this form of diagnostic testing can become mainstream and part of the clinical standard of care. �

 

Other promising advances have occurred in transcriptomics, proteomics and metabolomics. Host and microbial microRNA or miRNA, profiles have been utilized for a variety of inflammatory and infectious diseases. Two miRNAs, miR-155 and miRNA-29b, were reported as potential biomarkers for JEV infection and treatment targets for anti-JEV therapy. Host neural epidermal growth factor, including 2 and apolipoprotein B in CSF, was able to diagnose tuberculous meningitis with 83.3 percent to 89.3 percent sensitivity and 75 percent to 92 percent specificity. CSF metabolite profiling has been reported to be useful in the classification, diagnosis, epidemiology, and treatment assessment of CNS infections in HIV patients. CSF metabolic profile analysis demonstrated bioenergetic adaptation in regulating shifts of HIV-infected patients. �

 

Outcome Measures Associated with Diseases

 

Diagnosis of an etiologic agent in patients with CNS infections needs consideration of the most common causative organisms, the available diagnostic techniques and molecular methods for these agents, and the highest-yield clinical specimens for evaluation and testing. Knowledge of the epidemiology and clinical presentation of specific agents is fundamental in selecting which diagnostic methods are appropriate for patients. Animal or vector exposures, geographic location, recent travel history, season of the year, exposure of ill contacts, and occupational exposures should be considered. �

 

When selecting appropriate pathogen-specific molecular diagnostic methods, the following factors should be considered. CSF is the optimal specimen for PCR testing for patients with meningitis or meningoencephalitis. While indirect evidence can be determined by testing other specimen types, attempts should be made to obtain CSF samples early before treatment can compromise yield. Time of testing from the manifestation of symptoms is fundamental to understand and rule out false-negative results and recommend retesting within a certain time frame. By way of instance, HSV PCR can commonly render false-negative results if CSF sample is obtained very early or late in the process of HSE infection. Host health is also known to affect test performance characteristics. Immunocompromised patients are at risk for infection by a variety of opportunistic pathogens, by way of instance HHV-6, JC virus, Toxoplasma encephalitis in bone marrow transplant recipients and patients with HIV. Often, infection can be more severe, such as WNV, and challenging to diagnose in this population. Table 3 below demonstrates practical recommendations on application and pitfalls of molecular test for the diagnosis of CNS infections. �

 

Table 3 Molecular Methods in Detecting CNS Infections 1 | El Paso, TX Chiropractor Table 3 Molecular Methods in Detecting CNS Infections 2 | El Paso, TX Chiropractor

 

Furthermore, a positive nucleic acid amplification testing results are considered to be complicated by the fact that some viruses survive latently in macrophages or neurologic tissues even if they’re incidentally diagnosed by sensitive molecular techniques without an actual pathogenic role which can potentially lead to overtreatment. Utilization of adjunctive biomarkers which help determine active replication is being explored to overcome this drawback in research studies. �

 

Historically, the diagnosis of microbiologic agents in patients with CNS infections has been hindered by the low yield of CSF culture for viral and fastidious bacterial organisms, delays in CNS production of organism-specific antibodies, and challenges in determining optimum samples for testing. The nucleic acid in vitro amplification-based molecular diagnostic methods and techniques have a wider and better application in clinical microbiology practice. The monoplex assay will likely be the main platform utilized for urgent, random-access, low throughput assays. Multiplex assays have the additional benefit of diagnosing multiple targets and mixed infections. As the volume of CSF sample retrieved is often small, multiplex assays enable comprehensive diagnostic analysis with a low amount of sample, obviating the need for repeated lumbar punctures. The clinical relevance and cost-effectiveness of simultaneous multi-pathogen diagnosis strategies need further research studies. Application of pan-omic techniques in challenging to diagnose CNS infections is the new exciting frontier, the technology is promising but routine implementation is expected to be slow due to various challenges, such as lack of applicable regulatory guidelines and adaptation in the clinical setting, although the outcome measures are promising. �

 

As previously mentioned, central nervous system, or CNS, infections can be life-threatening health issues if they are not accurately diagnosed and properly treated. However, determining a diagnosis of CNS infections can be challenging for many clinicians. Fortunately, a variety of diagnostic techniques and molecular methods can ultimately help determine the source of CNS infections and other health issues. These diagnostic techniques and molecular methods have tremendously improved over the years, as previously mentioned, and more of these evaluations are being utilized in clinical settings to accurately diagnose CNS infections for proper treatment. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

In part 2 of our “Diagnosis of Central Nervous System Infections” article, we discussed the molecular methods and the pan-omic molecular assays which are utilized in the diagnosis of CNS infections as well as how specific testing outcome measures have ultimately been associated with clinical diseases and health issues. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Diagnosis of Central Nervous System Infections Part 1

Diagnosis of Central Nervous System Infections Part 1

The central nervous system, or CNS, plays a fundamental role in the pathogenesis of infection. The CNS is regulated by the blood-brain barrier or BBB, however, it can still be exposed to a microbial invasion from a contiguous focus, hematogenous dissemination, or intraneural passage of organisms. A variety of environmental or commensal bacteria, viruses, fungi, protozoa, or parasites can enter the CNS and cause a variety of infections and health issues. Central nervous system infections can ultimately cause headache, stiff neck, vomiting, fever, photophobia, and focal neurological symptoms. �

 

What are Central Nervous System Infections?

 

CNS infections are characterized according to their affected region. Infection of the brain, spinal cord, and meninges results in meningitis, encephalitis, brain abscess, and myelitis. Infections can affect single or multiple regions of the brain, such as meningoencephalitis and encephalomyelitis. Moreover, CNS infections are characterized as acute, sub-acute, chronic, or recurrent based on their duration. Meningitis can cause headache, neck stiffness, fever, and photophobia over a period of hours to days. Encephalitis can cause brain parenchymal inflammation which can ultimately cause lethargy to coma. Last but not least, Myelitis can cause inflammation of the spinal cord including headache, fever, and paraparesis or paralysis. �

 

Diagram of Central Nervous System and Pathogens.

 

One of the most fatal CNS infections, acute bacterial meningitis, with three to five cases for every 100,000 people in the United States, has a mortality rate of 6 percent to 26 percent. Approximately 4,000 cases of acute bacterial meningitis occur in the U.S. every year with about 500 deaths. The frequent cause of acute bacterial meningitis includes Streptococcus pneumoniae, group B Streptococcus, Neisseria meningitides, Haemophilus influenzae, and Listeria monocytogenes. �

 

CNS infections caused by viruses are more common and are mostly mild and self-limited. However, these can manifest as meningitis and/or encephalitis. CNS infections caused by viruses can vary due to region and season. Non-polio enteroviruses are responsible for the majority of meningitis and/or encephalitis cases from late spring to fall. CNS infections due to herpes simplex viruses, or HSV, are associated with sporadic encephalitis and meningitis with severe sequelae if left untreated. �

 

Diagnosis of CNS Infections

 

Diagnosis of microbial pathogens is fundamental for treatment. Methods and techniques utilized in clinical microbiology laboratories include direct microscopic examination, and culture techniques as well as antigen and antibody detection assays. However, each method and technique has several essential limitations. By way of instance, direct microscopic examination of CSF restricted sensitivity and specificity. The sensitivity of culture for enteroviruses is between 65 percent to 75 percent with average retrieval time of 3.7 to 8.2 days. Moreover, several serotypes of enteroviruses, especially Coxsackievirus A strains, are well-known to be non-cultivable and frequently grow poorly. Because enteroviruses are missing a common antigen found throughout a variety of serotypes, universal antigen and/or antibody diagnosis is impossible. Diagnosis of CNS HSV infections through methods and techniques utilized to determine culture sensitivity from CSF is tremendously poor. The presence of HSV IgG antibodies in CSF can ultimately be utilized to determine a diagnosis, however, the production is delayed until day 10 or day 12 after infection and it is not considered ideal for early diagnosis.

 

Methods and Techniques for Diagnosis of Central Nervous System Infections.

 

Diagnostic techniques, especially PCR based amplification, have developed a variety of mainstay tools to help determine the diagnosis of microbial pathogens in CSF. Molecular methods have demonstrated greater diagnosis rates than other diagnostic techniques. One research study demonstrated that 16S rRNA PCR-based assays were able to diagnose the causative organism in 65 percent of banked CSF samples compared to 35 percent when utilizing culture and microscopy. In another research study, diagnosis based on diagnostic techniques like molecular methods were utilized to optimize antibiotic treatment of patients with infectious meningitis when conventional methods and techniques demonstrated a negative outcome measure. Molecular methods and diagnostic techniques utilized on CSF samples are a fundamental standard when compared to the culture standard in the diagnosis of CNS infections caused by viruses which are challenging to diagnose. �

 

The diagnosis of CNS infections has tremendously changed over the last several years. PCR-based molecular methods have become a fundamental element in the clinical microbiology laboratory, providing tools for an accurate diagnosis. As demonstrated in Table 2, a variety of commercial molecular assays have been cleared by the Food and Drug Administration, or FDA, for the diagnosis of microbial pathogens. The approved assays for pathogen detection in the CNS are shown below. �

 

FDA Assays for Pathogen Detection in the CNS.

 

However, there are still several challenges in molecular diagnostic techniques and methods. Utilizing a combination of conventional diagnostic techniques and molecular methods, research studies demonstrated that in approximately 62 percent of patients with encephalitis, an etiologic organism could not be identified. Researchers have started to focus on developing advanced techniques and methods. In the following series of articles, we will demonstrate an update on the current conventional and molecular platforms utilized for the diagnosis of CNS infections. We will also demonstrate a preview on the potential clinical application of future technologies, including pan-omic assays. The emphasis of the following series of articles is to demonstrate optimal test selection in the clinical scenario for the diagnosis of CNS infection. �

 

Conventional Microbiology Methods and Techniques

 

Microscopic Examination

 

A positive CSF Gram stain confirms the diagnosis of bacterial meningitis. The sensitivity of the Gram stain for the diagnosis of bacterial meningitis is approximately 60 percent to 80 percent in patients not on antimicrobial treatment and approximately 40 percent to 60 percent in patients on antibacterial treatment. In one research study, Gram stain diagnosed as much as 90 percent Streptococcus pneumoniae and 50 percent Listeria monocytogenes in CSF collected from patients with bacterial meningitis confirmed by PCR 26 techniques and methods. Two organisms which are frequently diagnosed by microscopy include Mycobacterium tuberculosis by acid-fast bacillus, or AFB, staining and Cryptococcus neoformans by India ink or Gram stain. However,� the sensitivities of these techniques and methods are poor and culture is generally utilized instead. �

 

Culture

 

Culture of brain tissue can demonstrate a positive diagnosis of CNS infections, however, getting biopsies are tremendously invasive and frequently avoided unless a clinician determines that they are absolutely necessary. CSF sampling is most commonly performed to diagnose CNS infection. CSF viral, bacterial, including mycobacterial, and fungal cultures are fundamental in the diagnosis of infectious meningitis. However, CSF cultures in these cases are extremely low. Another disadvantage of CSF bacterial culture is that it generally requires up to 72 hours to determine a final diagnosis. A recent research study demonstrated that CSF mycobacterial culture had a sensitivity of 22 percent and a specificity of 100 percent in the diagnosis of tuberculosis meningitis. For viruses, utilizing monoclonal antibodies through culture increased the speed and specificity. However, due to time and sensitivity, CSF viral culture is frequently unable to determine a diagnosis. �

 

Rapid Antigen Detection

 

Cryptococcal antigen is the most commonly utilized antigen assay for CNS infections. The test utilizes Cryptococcus capsular polysaccharide antigens in CSF through enzyme immunoassay to determine a diagnosis. In a single research study which evaluated patients less than 35 years of age with CNS cryptococcosis, overall sensitivity and specificity of 93 percent to 100 percent and 93 percent to 98 percent were shown. Cryptococcus is a neurotropic fungus. Polysaccharide serum antigen titers with host immune status are frequently utilized to determine the need for a lumbar puncture to evaluate the patient for CNS health issues. The baseline peak titer of polysaccharide antigen in serum or CSF has demonstrated fundamental prognostic significance with an increased titer, or peak titer less than 1:1024, associated with antifungal therapy failure. �

 

The diagnosis of galactomannan, or GM, antigen and 1,3 ?-D-glucan, or BDG, in CSF, can help in the diagnosis of CNS aspergillosis or other invasive fungal infection such as fusariosis. Increased BDG in serum and CSF is associated with fungal infections. Measuring the levels of BDG is a beneficial biomarker in the evaluation of fungal CNS infection. It was recently demonstrated that patients receiving effective antifungal therapy demonstrated a decrease in CSF BDG concentrations with less than 31pg/ml and for this reason, BDG titers in CSF are a beneficial biomarker when monitoring response to treatment. �

 

For acute bacterial meningitis, a rapid antigen assay can help diagnose for a pneumococcal capsular antigen. Several research studies have demonstrated the utilization of M. tuberculosis-specific antigens in CSF for the diagnosis of tuberculosis meningitis. M. tuberculosis Early Secreted Antigenic Target 6, or ESAT-6, has been utilized for tuberculosis meningitis. �

 

Serology

 

Serological diagnosis of CNS infections is determined by identifying IgM antibodies or by demonstrating an increase in neutralizing antibody titers between acute- and convalescent-phase CSF. Due to a delay in antibody response when symptoms have manifested, a negative antibody test cannot be utilized to rule out infections and retesting may be required. Moreover, in specific populations, such as immunocompromised patients, the tests may not offer optimum sensitivity. In most instances, nucleic acid amplification tests have surpassed antibody-based detection as the test of choice. For several CNS infections, these assays play a fundamental role. CSF IgM is the most commonly utilized test for West Nile virus, or WNV, infections. Antibodies may manifest in as soon as 3 days and may continue for up to 3 months. However, its accuracy is challenged by high cross-reactivity with other flaviviruses and associated vaccines. Antibodies in recombinant WNV E proteins can determine where cross-reacting viruses co-circulate or determine which patients have been immunized. �

 

Fundamental serological assays for CNS infections are utilized for the diagnosis of neurosyphilis. Neurosyphilis is determined by a positive CSF venereal disease research laboratory, or VDRL, test. Diagnosis of varicella-zoster virus, or VZV, IgG in CSF is the most common technique and/or method for the diagnosis of VZV associated with CNS infection. �

 

Central nervous system, or CNS, infections can ultimately be life-threatening health issues if they are not diagnosed and treated early. Determining an accurate diagnosis of CNS infections can be challenging. Fortunately, a variety of diagnostic techniques and molecular methods can help determine the source of CNS infections. These diagnostic techniques and molecular methods have tremendously improved over the years and more and more of these evaluations are being utilized in clinical settings to accurately diagnose CNS infections for early treatment. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

In part 2 of our “Diagnosis of Central Nervous System Infections” article, we will ultimately discuss the molecular methods and the pan-omic molecular assays which are utilized in the diagnosis of CNS infections as well as discuss how specific testing outcome measures are associated with clinical diseases and health issues. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �

 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

What is Mitochondrial Disease?

What is Mitochondrial Disease?

Mitochondria are the “energy factory” of the human body. Several thousand mitochondria can be found in nearly every cell. Mitochondria also play several fundamental roles in the body, such as converting chemicals from the foods we eat into energy as well as to process oxygen. Mitochondria produce 90 percent of the energy the human body requires to function accordingly. The purpose of the following article is to describe an overview of mitochondrial disease and well-being. �

 

What are Mitochondrial Diseases?

 

Mitochondrial diseases are characterized as chronic, genetic, and often inherited health issues which ultimately occur when mitochondria fail to produce enough energy for the human body to function properly. Mitochondrial diseases may develop from birth however they can frequently develop at any age. Mitochondrial disease can affect any region of the human body, including the cells of the brain, muscles, heart, liver, kidneys, pancreas, eyes, ears, and nerves, among other structures. �

 

When the mitochondria don’t function as well as they should because of another health issue, mitochondrial dysfunction occurs. Furthermore, many health issues can cause secondary dysfunction and result in other neurological diseases, such as Alzheimer’s disease, Lou Gehrig’s disease, and muscular dystrophy. People with secondary dysfunction don’t have genetic mitochondrial disease and do not need to be concerned about the ongoing development or worsening of symptoms. �

 

What are the Symptoms of Mitochondrial Disease?

 

Symptoms of mitochondrial disease depend on which cells of the human body are affected. Symptoms can develop at any age, involve one or more organs, and may range from mild to severe. Even patients within the same household, having the exact same mitochondrial disease can have gaps in symptoms, severity, and age of onset or beginning of symptoms. �

 

Symptoms of mitochondrial diseases can include: �

 

  • Poor growth
  • Muscle pain, muscle weakness, exercise intolerance, low muscle tone
  • Vision and/or hearing problems
  • Learning disabilities, delays in development, mental retardation
  • Autism, autism-like features
  • Heart, liver or kidney diseases
  • Gastrointestinal disorders, swallowing difficulties, constipation or diarrhea, vomiting, cramping, acid reflux
  • Diabetes
  • Increased risk of infection
  • Neurological problems, seizures, migraines, strokes
  • Movement disorders
  • Thyroid problems
  • Respiratory problems
  • Lactic acidosis or a buildup of lactate
  • Dementia

 

What are the Causes of Mitochondrial Disease?

 

In many people, primary mitochondrial disease is a genetic health issue which can be inherited in several ways. To understand inheritance types, it is helpful to find out more about genes and DNA. Genes are substances which provide us our traits, like brown eyes or blue eyes. Genes contain DNA, which is the “blueprint” which gives each person their distinctive make-up. �

 

In normal circumstances, a child inherits one gene from the father and one gene from the mother. A child with a mitochondrial disease doesn’t receive the pair of genes from the parents. The gene has mutated or has become defective. Learning how the mitochondrial disease is inherited helps predict the prospect of passing the disease(s) to children. �

 

Inheritance types of mitochondrial disease are: �

 

  • Autosomal recessive inheritance: The child receives one mutated copy of a gene from each parent. There is a 25 percent chance that each child in the family will inherit a mitochondrial disease.
  • Autosomal dominant inheritance: The child receives one mutated copy of a gene from either parent. There is a 50 percent chance that each child in the family will inherit a mitochondrial disease.
  • Mitochondrial inheritance: In this unique type of inheritance, the mitochondria contain their own DNA. Only mitochondrial disorders caused by mutations in the mitochondrial DNA are exclusively inherited from mothers. There is a 100 percent chance that each child in the family will inherit a mitochondrial disease.
  • Random mutations: Occasionally, genes develop a mutation of their own which is not inherited from a parent.

 

How are Mitochondrial Diseases Diagnosed?

 

Mitochondrial diseases can be difficult to diagnose by a healthcare professional because mitochondrial diseases can ultimately affect a variety of organs and tissues in the human body and patients can also have a variety of symptoms. There is currently no single lab test or diagnostic test which can confirm the identification of mitochondrial disease. That is why a referral to a medical facility with healthcare professionals who focus on these diseases is essential to making the diagnosis. �

 

Diagnosis begins with a series of evaluations and tests which may include: �

 

  • A review of a patient�s family history
  • A complete physical evaluation
  • A neurological evaluation
  • A metabolic evaluation which includes blood and urine tests, and, if needed, a cerebral spinal fluid test

 

Other evaluations, determined by the regions of the human body and the patient’s symptoms which may include: �

 

  • Magnetic resonance imaging (MRI) or spectroscopy (MRS) for neurological symptoms
  • Retinal exam or electroretinogram (ERG) for vision symptoms
  • Electrocardiogram (EKG) or echocardiogram for symptoms of heart disease
  • Audiogram or auditory-brainstem evoked responses (ABER) for hearing symptoms
  • Blood test to detect thyroid dysfunction if the patient has thyroid problems
  • Blood test to perform genetic DNA testing

 

Testing may include biochemical testing. Biopsies of skin and muscle tissue may also be utilized for diagnosis. �

 

How are Mitochondrial Diseases Treated?

 

Unfortunately, there is no cure for mitochondrial disease, however, treatment can help reduce symptoms or slow the decline of overall well-being. Treatment varies from patient to patient and depends on the severity and the mitochondrial disease characterized. There is absolutely no way to predict a patient’s reaction or forecast how that person will be affected in the long-term. No two people respond the same way to the same treatment even if they have the same mitochondrial disease. �

 

Treatments for mitochondrial disease may include: �

 

  • Vitamins and supplements, including Coenzyme Q10; B complex vitamins, such as thiamine (B1) and riboflavin (B2), Alpha lipoic acid, L-carnitine (Carnitor), Creatine, and L-Arginine.
  • Exercise and physical activity, including endurance exercises and resistance/strength training to increase muscle strength. Endurance exercises include walking, running, swimming, dancing, cycling and others. Resistance/strength training includes exercises such as sit-ups, arm curls, knee extensions, weight lifting and others.
  • Conserving energy. Don�t try to do too much in a short period of time. Pace yourself.
  • Other treatments including speech therapy, respiratory therapy, physical therapy, and chiropractic care, among others.

 

Avoid situations which can make the health issue worse. This includes exposure to cold and/or warmth, starvation, lack of sleep, stressful situations, and usage of alcohol, smokes and monosodium glutamate or MSG, a flavor enhancer commonly added to Chinese foods, canned vegetables, soups, as well as processed meats, among other processed foods. �

 

Mitochondrial diseases are long-term, genetic, and frequently inherited health issues which occur when the mitochondria fail to produce enough energy for the human body to function accordingly. According to research studies, approximately one in 5,000 people has a genetic mitochondrial disease. Chiropractic care is an alternative treatment option which can help relieve symptoms associated with a variety of health issues, including mitochondrial diseases. Many chiropractors are qualified and experienced in the treatment of neurological diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The purpose of the article above is to describe mitochondrial disease and its effect on overall health and wellness. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

What is Cerebral Perfusion Pressure?

What is Cerebral Perfusion Pressure?

Cerebral perfusion pressure, or CPP, is the net pressure gradient which carries oxygen to brain tissue. It is measured by the difference between the mean arterial pressure, or MAP, and the Intracranial Pressure, or ICP,� which is measured in millimeters of mercury (mm Hg). Regulating CPP is fundamental in the treatment of patients with intracranial pathology, including shock, hemodynamic distress, and traumatic brain injury. �

 

Although the average CPP is generally between 60 and 80 mm Hg, these values may change to the left or to the right depending on individual physiology. MAP and ICP has to be measured together because CPP is a calculated measure. Regulating CPP at hemodynamically unstable conditions with abnormal ICP or in cases of intracranial pathology will reduce the chance of ischemic brain injury. �

 

  • CPP = MAP – ICP

 

Cerebral Perfusion Pressure Physiology

 

CPP and ICP

 

At its own average range of 60 to 80 mm Hg, the CPP is determined by the ICP and the mean arterial pressure. Under regular standards, the ICP is between 5 and 10 mm Hg which has a reduced effect on the CPP than the MAP in clinical circumstances not associated with intracranial pathology. ICP is generally measured through intracranial pressure transduction.

 

Physiologically, the ICP is a function of intracranial compliance. Intracranial compliance is the relationship between the ICP and the volume of the intracranial cavity including cerebrospinal fluid, or CSF, brain tissue as well as arterial and venous blood volume. Because the skull is a fixed and rigid anatomic space, the ICP can increase if the intracranial volume increases while intracranial compliance decreases. As the ICP increases or intracranial compliance decreases, CPP also decreases. �

 

Several processes determine that ICP continues to stay within the average range for the longest extended period of time possible, especially throughout periods of affected intracranial volume and compliance. As volume adds to the intracranial space, CSF can shift into the spinal subarachnoid space, causing the ICP to continue significantly unchanged. As volume increases due to a growing space-occupying lesion, brain tissue edema or blood, this process ultimately becomes overwhelming, and ICP begins to increase substantially. �

 

Cerebral blood flow, or CBF, is also a fundamental factor in ICP homeostasis. Cerebral auto-regulation makes sure that steady blood flow is maintained in the brain over a wide range of physiologic alterations. When blood pressure decreases, auto-regulation causes cerebral vasodilation and an increase in CBF and cerebral blood volume, maintaining ICP and CPP. However, when blood pressure increases, auto-regulation causes cerebral vasoconstriction and a decrease in CBF with a decrease in cerebral blood volume, also regulating ICP and CPP. Too many changes outside of average CBF ranges can cause brain ischemia and injury. �

 

CPP and MAP

 

Because ICP in its average ranges is a considerably small number, the CPP generally depends on the mean arterial pressure. MAP is the normal blood pressure during one cardiac cycle which can be measured through invasive hemodynamic monitoring or calculated by the systolic blood pressure, plus two times the diastolic blood pressure, divided by three. The average range of MAP is 70 to 100 mm Hg. �

 

The average arterial pressure can be affected due to everyday activities, such as rest, stress, and exercise or physical activities. However, if the ICP continues to stay the same, the average arterial pressure can change across its significantly wide range without tremendously decreasing or increasing the CPP. As a matter of fact, CPP and CBF will continue to stay considerably unchanged across a wider range of MAP (50 � 150 mm Hg) than normal due to cerebral auto-regulation and vasoconstriction or vasodilation of cerebral vasculature. �

 

For patients with hypertension, the auto-regulation setpoint changes, decreasing the average arterial pressure associated with the patient�s normal arterial pressure, which causes vasodilation to increase CBF. Patients with lower than normal average arterial pressure at baseline will have auto-regulatory vasoconstriction as a reaction to an increase in their significant average MAP, to return CBF to baseline. When looking at CBF and CPP in the context of the patient�s average MAP, it is clinically significant based on the regulation of intracranial pathology and hemodynamic derangements. �

 

Cerebral Perfusion Pressure Complications

 

Diagnosing and treating cerebral perfusion pressure complications necessitates measuring both the ICP and the MAP. The MAP may be quantified through the utilization of invasive hemodynamic processes, most frequently cannulation of a peripheral artery such as the radial or femoral artery. The MAP may also be measured with a non-invasive blood pressure cuff by applying the formula mentioned above utilizing the systolic and diastolic blood pressures. � Intracranial pressure is generally measured through an intracranial pressure transduction device. The most common and most accurate method or technique is utilizing an intraventricular monitor. The intraventricular dimension of ICP is the normal standard. An intraventricular catheter is inserted into a hole drilled in the skull and into the lateral ventricle to gauge the pressure of the CSF. The benefit of an intraventricular catheter is that CSF could be eliminated, if needed, to decrease ICP. Considerable complications for the ICP include a possibility of bleeding, infection, and difficulty with proper placement. Options include sub-dural and intra-parenchymal monitors. �

 

The ICP can be measured non-invasively through several methods and techniques, including transcranial Doppler ultrasonography or TCD. TCD utilizes a temporal window to evaluate the speed of blood flow through the middle cerebral artery. Systolic and diastolic average flow velocity is utilized to determine a pulsatility index. The pulsatility index was determined to be closely associated with ICP in several research studies as well as be associated with ICP in other research studies. Therefore, it is not suggested to use TCD as a substitute for direct ICP dimension. Invasive diagnosis and treatment of the MAP through an arterial cannula and the ICP through an intraventricular catheter will give a continuous and accurate calculation of CPP. �

 

Cerebral Perfusion Pressure Clinical Significance

 

Two general types of pathologic health issues can ultimately occur where the regulation of the CPP is fundamental, such as intracranial pathology, where ICP regulation is essential and hemodynamic instability/shock where MAP regulation is the most essential. Intracranial pathology involves space-occupying lesions, such as tumors, epidural and subdural hematoma or severe intraparenchymal hemorrhage and cerebral edema as seen after ischemic injury, traumatic brain injury or acute hepatic encephalopathy. In these circumstances, average CPP depends on decreasing the ICP into a normal range as soon as possible while regulating the MAP. When CPP is normal, it’s fundamental to keep in mind that every individual’s brain tissue has a CPP that is “normal” in the context of that individual patient’s physiology, which may be affected by other health issues, such as hypertension or cardiovascular disease. Moving towards a more dynamic direction of the average CPP utilizing the patient’s personal auto-regulatory capacity. These diagnosis and treatment approaches involve more frequent and sophisticated monitoring and might not be readily available for widespread utilization. �

 

In the instance of considerable traumatic brain injury, significant cerebral edema can decrease intracranial compliance and CSF, developing an increased ICP or intracranial hypertension. Auto-regulatory mechanisms and techniques may or may not function normally and when ICP continues to be elevated, CPP will decrease causing further injury through an ischemic process. In circumstances such as these, together with starting the measures for decreasing the ICP, it is essential to prevent hypotension (MAP – ICP = CPP) and in some instances, allowing hypertension to reasonably occur. �

 

In circumstances of instability, the ICP is considerably stable as cerebral auto-regulation is undamaged. In the instance of hypotension, the MAP decreases due to blood loss, or hemorrhagic shock, intravascular leak, or distributive shock, and decreased cardiac output, or cardiogenic shock, and the CPP also decreases. It’s the association between MAP and CPP which carries resuscitation guidelines to recommend regulating a MAP greater than or equal to 65 mm Hg. With a normal ICP, this threshold must make sure that a CPP of 55 to 60, the minimum necessary to stop cerebral ischemic injury, is ultimately maintained. As in the circumstance of ICP and cerebral auto-regulation, the goal of MAP is to be within the context of an individual patient’s evaluation hemodynamic function. Patients with untreated hypertension must have increased MAP goals to maintain proper CBF and CPP. �

 

As previously mentioned in the following article, cerebral perfusion pressure, or CPP, is the net pressure gradient which affects cerebral blood flow to the brain, also known as brain perfusion. According to healthcare professionals, the CPP, or cerebral perfusion pressure, must be constantly regulated within a specific limit because too little pressure or too much pressure could potentially cause a variety of brain health issues. Cerebral perfusion pressure may be associated with a variety of neurological diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The purpose of the article is to discuss cerebral perfusion pressure and its association with neurodegenerative diseases. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

What is the Role of Glial Cells?

What is the Role of Glial Cells?

You have probably heard about the “gray matter” of the brain which is made up of cells known as neurons, however, a lesser-known type of brain cell is ultimately what makes up the “white matter” of the brain.� These are known as glial cells. �

 

Glial cells, also known as glia or neuroglia, were only considered to simply offer structural support. The term “glia” literally translates to “neural adhesive.” However, relatively recent research studies have demonstrated that they play a variety of roles in the brain and the nerves which run throughout the entire human body. However, there is more left to find out. �

 

Types of Glial Cells

 

Glial cells commonly offer support to the neurons. Without them, several of the most fundamental roles would never be achieved although they may not perform these roles themselves. Glial cells come in numerous forms, each of which performs certain functions to keep the brain functioning properly or not, in case of a neurological disease which affects the glial cells. �

 

The central nervous system, or CNS, is made up of the brain, the spinal cord, and the nerves. Five types of glial cells include: �

 

  • Astrocytes
  • Oligodendrocytes
  • Microglia
  • Ependymal cells
  • Radial glia

 

Moreover, there are also glial cells on the peripheral nervous system, or PNS, which is made up of the nerves in the upper and lower extremities, away from the spine. The two types of glial cells found in the peripheral nervous system include: �

 

  • Schwann cells
  • Satellite cells

Glial Cells Diagram | El Paso, TX Chiropractor

Astrocytes

 

The most common type of glial cell in the central nervous system is the astrocyte, also known as astroglia. The “astro” part of the name refers to how they look like stars with projections coming out all over the glial cell. Protoplasmic astrocytes have thick projections with lots of branches. Fibrous astrocytes have long, slender arms. The fibrous ones are found in the white matter while others are found among neurons in the gray matter.� Astrocytes play several major roles, including: �

 

  • Developing the blood-brain barrier or BBB. The BBB is similar to a strict security system which only allows substances which are supposed to be in the brain. This filtering system is essential for maintaining brain health.
  • Regulating the substances around neurons. Neurons communicate utilizing chemical messengers known as neurotransmitters. Once a chemical has transmitted a message to a cell, it essentially stays there cluttering things up until an astrocyte recycles it through a process known as reuptake. The reuptake process is generally the main target of numerous medications, including anti-depressants. Astrocytes also clean up what’s left behind when a neuron dies, as well as excess potassium ions, which are chemicals that play a fundamental role in nerve function.
  • Regulating blood flow to the brain. For the brain to process information accordingly, it needs a certain amount of blood to flow throughout all of its different regions. An active region receives more blood flow than an inactive one.
  • Synchronizing the activity of axons. Axons are characterized as long, thread-like elements of the neurons and the nerve cells which ultimately conduct electricity to help transmit messages from one cell to another.

 

Astrocyte dysfunction has been potentially connected to a wide variety of neurological diseases, including: �

 

  • Amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease)
  • Huntington’s chorea
  • Parkinson’s disease

 

Animal models of astrocyte-related disorders are helping researchers learn more about these neurological diseases. �

 

Oligodendrocytes

 

Oligodendrocytes develop from stem cells. The term is made up of Greek words which, all together, mean “cells with several branches.” Their main role is to help information move faster. Oligodendrocytes appear like white spikey balls. Their purpose is to make a protective layer, similar to the plastic insulation on electric wires. This layer is known as the myelin sheath. �

 

The myelin sheath is not constant. There is a gap between each membrane which is known as the”node of Ranvier,” and it is the node which helps electrical signals move effectively along neural cells. The signal is transmitted from one node to the next, which increases the velocity of the nerve conduction whilst also reducing how much energy it takes to transmit it. �

 

Messages along myelinated nerves may travel as fast as 200 miles per second. At birth, you only have a few myelinated axons, and the quantity of these keeps growing until you’re about 25 to 30 years old. Myelination is thought to play an important role in intelligence. Oligodendrocytes also supply stability and transmit energy from blood cells into the axons. �

 

The expression “myelin sheath” may be familiar to you because of its association with multiple sclerosis. In multiple sclerosis, it is believed that the human body’s immune system attacks the myelin sheaths, which leads to the breakdown of these neurons and ultimately causes impaired brain functioning. Spinal cord injuries may also cause damage to these structures. � Other neurological diseases believed to be associated with oligodendrocyte dysfunction include: �

 

  • Leukodystrophies
  • Tumors known as oligodendrogliomas
  • Schizophrenia
  • Bipolar disorder

 

Several research studies suggest that oligodendrocytes may become affected by the neurotransmitter glutamate, which, among other functions, stimulates regions of the brain so that you’re able to focus and learn new information. Nonetheless, in high levels, glutamate can be considered an “excitotoxin,” which means that it may overstimulate cells until they die. �

 

Microglia

 

Microglia are tiny glial cells. They act as the brain’s dedicated immune system, which is necessary since the BBB isolates the brain from the rest of the human body. Microglia are attentive to indications of disease and injury. If they find a problem, they are in charge of taking care of it, even if it ultimately means clearing away dead cells or getting rid of a toxin or pathogen. �

 

If they respond to an injury, microglia cause inflammation as part of the recovery process. In some cases, such as in Alzheimer’s disease, they might become hyper-activated and cause too much inflammation. That is thought to cause amyloid plaques and other health issues connected with the neurological disease, among a variety of other brain health issues. � Along with Alzheimer’s disease, other neurological diseases which may be associated with microglial malfunction include: �

 

  • Fibromyalgia
  • Chronic neuropathic pain
  • Autism spectrum disorders
  • Schizophrenia

 

Microglia have been thought to play many fundamental roles beyond that, including learning-associated plasticity and guiding the development of the brain. The brain produces many connections between neurons which allow them to pass information back and forth. The brain produces a lot more of these than we need, which is not always efficient. �

 

Microglia detect unnecessary synapses and they clean them out. Microglial research has really taken off in recent decades, leading to an ever-increasing comprehension of their roles in both health and disease in the central nervous system. �

 

Ependymal Cells

 

Ependymal cells are primarily known for creating a membrane known as the ependyma, and it can be described as a thin membrane lining the central canal of the spinal cord and the ventricles or passageways of the brain. They also create cerebrospinal fluid. Ependymal cells are extremely small and they lineup closely together to make the membrane. �

 

Inside the ventricles, are the cilia, which look like small hairs which move back and forth to help circulate the cerebrospinal fluid. Cerebrospinal fluid provides nutrients and removes waste products in the brain. Additionally, it serves as a cushion and shock absorber between the skull and the brain. It’s also essential for homeostasis in the brain, regulating its temperature along with other attributes which keep its potential and functioning. Ependymal cells are also included in the BBB. �

 

Radial Glia

 

Radial glia are believed to be a type of stem cell, which means that they create other types of cells. In the developing brain, they’re the”parents” of neurons, astrocytes, and oligodendrocytes. They also supply scaffolding for developing neurons, thanks to long fibers which direct young brain cells into position as the brain forms in a human embryo. Their role as stem cells, especially as founders of neurons, is ultimately what makes them the focus of research studies regarding how to repair brain damage from injury or illness. Later in life, the radial glia perform important roles in neuroplasticity as well. �

 

Schwann Cells

 

Schwann cells are known after the physiologist Theodor Schwann, who discovered them. They function a lot like oligodendrocytes in which they supply myelin sheaths for axons, but they develop in the peripheral nervous system, or PNS, rather than in the central nervous system or CNS. However, Schwann cells form spirals directly across the axon. �

 

Ranvier’s nodes are found between the membranes of oligodendrocytes and these help in neural transmission in precisely the same exact way. Schwann cells can also be part of the PNS’s immune system. They ultimately have the ability to consume the axons of the nerve and give a protected path for a brand new axon to develop when another nerve cell is damaged. Neurological diseases involving abnormal Schwann cells include: �

 

  • Guillain-Barre’ syndrome
  • Charcot-Marie-Tooth disorder
  • Schwannomatosis
  • Chronic inflammatory demyelinating polyneuropathy
  • Leprosy

 

Several research studies on bronchial Schwann cells for spinal cord injury and other types of peripheral nerve damage have been promising. Schwann cells are implicated in certain types of chronic pain. Their activation following nerve damage may contribute to dysfunction in a type of nerve fiber known as nociceptors, which feel external factors like heat and cold. �

 

Satellite Cells

 

Satellite cells get their name due to the way they surround certain neurons, with several satellites forming a sheath around the cellular surface. Researchers have only just started to learn about these cells but they’re believed to be similar to astrocytes. The main role of satellite cells is believed to be the regulation of the surroundings around the nerves. �

 

The nerves which have satellite cells make up something known as ganglia, which are clusters of nerve cells in the autonomic nervous system and sensory apparatus. The autonomic nervous system regulates internal organs, even while the sensory system is what enables people to see, hear, taste, touch, and smell. Satellite cells provide nourishment to the neuron and absorb heavy metal toxins, such as lead and mercury, to stop them from damaging the nerves and other structures. �

 

They are also believed to assist transport several neurotransmitters and other substances, including: �

 

  • Glutamate
  • GABA
  • Norepinephrine
  • Adenosine triphosphate
  • Substance P
  • Capsaicin
  • Acetylcholine

 

Much like microglia, satellite cells detect and respond to injury and inflammation. However, their role in repairing cell damage isn’t yet fully well understood. Satellite cells have been connected to chronic pain between peripheral tissue injury, nerve damage, and a systemic heightening of pain, or hyperalgesia, which can ultimately result from chemotherapy. �

 

Glial cells, also known as glia or neuroglia, are characterized as non-neuronal cells which are ultimately found in the central nervous system, or CNS, and the peripheral nervous system, or PNS. There are various types of glial cells, including astrocytes, oligodendrocytes, microglia, ependymal cells, and radial glia in the CNS and Schwann cells and satellite cells in the PNS. The glial cells play many fundamental roles in the human nervous system. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The purpose of the article is to discuss the types of glial cells associated with the brain and neurodegenerative diseases. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

� For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

Apoptosis in Neurological Diseases

Apoptosis in Neurological Diseases

Neural cell death can occur both during the development and throughout the pathophysiology of the nervous system. Two different types of cell death, known as necrosis and apoptosis, are involved in pathological neuronal loss, however, apoptosis is the process of programmed cell death during development. All types of cells will go through apoptosis. This mechanism controls neuronal growth where an excess of neurons is produced and only those which form connections with the target structures will receive enough survival factors. The remaining neurons will then ultimately go through death and removal. �

 

Apoptosis continues throughout life and it is the main process involved in the elimination of surplus, unwanted, damaged or aged cells. Dysregulation of apoptosis is demonstrated after damage or injury as well as in neurodegeneration and in tumorigenesis. Treatment approaches which influence the apoptotic pathway offer valuable therapeutic options in a wide variety of pathological states. The purpose of the article is to describe the significance of apoptosis in neurological diseases. �

 

What is Apoptosis?

 

Apoptosis is the well-conserved and highly controlled process of cell death involved in the removal of unnecessary, surplus, aged or damaged cells. Dysregulation of apoptosis can ultimately develop mutated cells which can result in malformations, autoimmune diseases, and even cancer. Abnormal apoptosis can also result in the elimination of healthy cells which can occur in health issues such as infection, hypoxic-ischaemic injury, neurodegenerative or neuromuscular diseases, and AIDS. �

 

Apoptosis is different from necrotic cell death. In necrosis, cell death is caused by an external factor and involves the early loss of tissue, damage to organs, and the leakage of cytoplasmic contents, leading to the recruitment of phagocytes which can cause an acute inflammatory reaction. In contrast, apoptosis is often considered cell suicide. According to research studies, cells which die due to apoptosis retain membrane and organelle structure and function until late in the process while still developing plasma membrane blebbing, reduced cytoplasmic volume, chromatin condensation, and nuclear fragmentation. �

 

In the final phases, cell fragments wrapped in plasma membrane pull away as apoptotic bodies which are then phagocytosed by healthy cells. The removal of cell debris also occurs in the absence of an inflammatory response, and this silent, quick, and efficient elimination of apoptotic cells mean that apoptosis can be difficult to find in cells. However, as many as 50 percent of the cells in developing adulthood may go through apoptosis where less than 1 percent of cells are apoptotic at any one time. �

 

Apoptosis in the Nervous System

 

Programmed cell death by apoptosis occurs in several developmental processes, such as body sculpting and removal of self-reacting resistant cells as well as sexual organ growth and gamete formation. The general principle of growth in multicellular organisms involves the development of excess numbers of cells, where the excess or unwanted cells are then removed by apoptosis through the development of functional organs. In the developing nervous system, apoptosis has been demonstrated to occur in neural tube formation and continues throughout terminal differentiation of the neural system. �

 

A growing number of neurotrophic factors, such as nerve growth factor family, including both the neurokines and development factors like insulin-like growth variables (IGF-I and IGF-II), encourage the survival of several types of neurons. Targeted disruption of genes encoding these factors or their receptors demonstrate that neurotrophic factors are significant for the development of specific neuronal populations. Neurotrophic factors function by binding to specific receptors in the cell membrane. Moreover, the effects of NGF offer a good illustration of the subtle command the system permits. �

 

The nerve growth factor receptor has high and low affinity components. It will function as a survival factor if it binds to the high-affinity trkA receptor but it will also cause apoptosis of retinal neurons or oligodendrocytes once it binds to the low-affinity receptor p75 in the absence of trkA. Nerve growth factor in the extracellular environment is consequently able to control neural development by both boosting the growth of several types of cells as well as the removal of other cells. �

 

In some cases, however, concentrated genetic disruption of neurotrophic factors or their receptors may leave the central nervous system seemingly unaffected, demonstrating that these variables can ultimately become biased. According to research studies, it has now become evident that the control of neuronal survival does not only depend on the supply of trophic molecules by the targets but also on activity, humoral factors, and trophic support from glia or glial cells. �

 

Furthermore, neurons don’t simply undergo programmed cell death during differentiation. Apoptosis appears to regulate cell numbers in systems as diverse as the disappearance of the germinal layer during the third trimester of pregnancy, the sexual differentiation of the medial preoptic nucleus where apoptosis is controlled by testosterone, lineages throughout the olfactory epithelium, oligodendrocyte development in the optic nerve, and the development of Schwann cells in the peripheral nervous system. Programmed cell death occurs in a variety of other processes in the developing nervous system. �

 

Apoptosis in Nervous System Injuries & Diseases

 

Although apoptosis is a fundamental process involved in the developing nervous system, apoptosis can ultimately be involved in a variety of nervous system injuries and diseases. In most cases, the connection between a specific mutation or trauma as well as the activation of apoptotic cascades remains evasive. An overview of a developing list of neurological diseases in which apoptosis has been implicated as a significant pathological mechanism is provided below. �

 

Neuronal Injury

 

Cerebral hypoxic-ischaemic injury is a cause of neurological injury and death. Magnetic resonance spectroscopy studies have demonstrated that transient hypoxia-ischemia contributes to a biphasic disturbance of cerebral energy metabolism. Related to the biphasic energy collapse, two waves of cell death appear to follow hypoxic-ischaemic injury in the developing brain. Immediate neuronal death is most likely due to necrosis resulting from the accumulation of calcium ions. �

 

Delayed cell death caused by hypoxic-ischemic injury appears to involve further mechanisms with increasing data which demonstrates that in the delayed phase, cell death occurs by apoptosis. The amount of apoptosis is directly associated with the magnitude of ATP depletion during hypoxia-ischemia. Apoptosis can occur in the brains of newborn babies following birth asphyxia and sudden intrauterine death. Apoptosis can also be notable in white matter injury in newborn babies. �

 

Apoptosis may continue for months after an hypoxic-ischaemic injury due to constant changes in cerebral energy metabolism in infants during the months after birth asphyxia. Following focal neural injury, apoptosis has been discovered in remote regions from the initial damage. After severe spinal cord injury in reptiles, apoptosis of oligodendrocytes occurs in distant degenerating fiber tracts and after forebrain injury in rats, apoptosis was demonstrated in the cerebellum. �

 

The apoptotic loss of oligodendrocytes could consequently be a potential source of secondary demyelination in paraplegia and in the chronic degeneration related to multiple sclerosis. Further research studies must be performed in order to provide further evidence on the role of apoptosis in this type of injury which begins from the report of which Bcl-2 expression boosts the growth and regeneration of retinal axons. Apoptosis in neuronal injury can be demonstrated in a variety of ways. �

 

Neural Cancers

 

A connection between apoptosis and the cell cycle is demonstrated in carcinogenesis where proto-oncogenes, such as c-fos, c-jun, and c-myc, can activate apoptosis and promote cell division while inactivation of the pro-apoptotic p53 tumor suppressor gene is a frequent mark of human neoplasia. By way of instance, in a number of gliomas, the reduction of wild p53 activity was connected to tumor progression, possibly leading to resistance to chemotherapy and radiotherapy. �

 

Although there have been reports of Bcl-2 overexpression in glioma cell lines, the correlation between the anti-apoptotic effect of this gene and malignancy is not yet clear. However, a homolog of Bcl-2, the brain associated apoptosis gene (BRAG-1), is found predominantly in the brain, and it is upregulated in human gliomas as a rearranged transcript. As demonstrated above, the process of apoptosis can also be significant in the development of neural cancers, according to research studies. �

 

Infectious Disease

 

Apoptosis may play a role in HIV encephalopathy. In the brain, the virus reproduces primarily in microglia which it enters through the CD4 receptor. Although the activation of microglia is believed to be the main reason for adrenal loss and demyelination, neurons die by apoptosis in HIV encephalopathies because of HIV mediated alterations in astrocyte function and aberrant stimulation of NMDA receptors or due to nitric oxide from the activation of inducible nitric oxide synthase. �

 

In subacute sclerosing panencephalitis, widespread apoptotic death was demonstrated to develop in the brain, although no correlation was observed between viral load, lymphocyte infiltration, and the number of apoptotic cells. DNA fragmentation indicative of apoptosis was detected in scrapie-infected sheep and mice brains, suggesting a function associated with cell death in spongiform encephalopathies. Apoptosis may also ultimately be involved in another infectious disease. �

 

Neurodegeneration

 

Spinal muscular atrophy is associated with mutations in the survival of motor neuron and neuronal apoptosis inhibitory protein (NAIP) enzymes. NAIP is closely related to the baculovirus inhibitor of apoptosis protein and inhibits apoptosis in many cell types. This implies that mutations in NAIP could deregulate apoptosis in spinal motor nerves, causing their death. Recent studies emphasize the importance of anti-apoptotic genes in cerebral protection which can rescue neurons. �

 

Apoptosis has also been implicated in retinal dystrophies such as retinitis pigmentosa. In this case, apoptosis results from mutations in the three photoreceptor genes, rhodopsin, peripherin, and the ?-subunit of cyclic guanosine monophosphate di esterase, resulting in photoreceptor degeneration. The absence of c-fos prevents apoptosis in those cells is unknown. Moreover, defined neurotrophins and growth factors injected intraocularly in animal models of retinal degeneration improve photoreceptor survival, suggesting that the apoptotic cascade can be obstructed by supplying exogenous survival signs. �

 

The mutation underlying Huntington’s disease is an expanded trinucleotide which is fundamental for normal development and can be regarded as a cell survival gene. Transgenic models demonstrated increased apoptosis in the neurons of an embryonic neuroectoderm. During apoptosis, caspase-3 (apopain) is improved by a gain of function associated with the triplet expansion. This is supported by the overexpression of specific trinucleotide repeats in transgenic mice. �

 

Most cerebellar ataxias are associated with neuronal loss. Ataxia-telangiectasia, caused by mutations in the ATM gene, is considered to have an apoptotic component. ATM shares extensive and significant homology with the DNA dependent protein kinases involved in DNA damage responses at different cell cycle checkpoints and is downregulated in most patients with ataxia-telangiectasia. The simple fact that inappropriate p53 mediated apoptosis is the major cause of death in ataxia-telangiectasia cells suggests that the mutation causes improper triggering of apoptosis by otherwise non-lethal DNA injury. �

 

From the familial form of amyotrophic lateral sclerosis gain of function, mutations in the gene encoding copper-zinc superoxide dismutase (sod-1) develop a dominant pro-apoptotic sign. Although cell harm by the accumulation of free radicals can trigger apoptosis, these mutants can induce apoptosis both in nerve cells in culture and in transgenic mice. Mental retardation in Down’s syndrome has also been associated with abnormal apoptosis. Although cortical neurons from fetal Down’s syndrome brains are different, they then degenerate and undergo apoptosis, according to research studies. �

 

Degeneration is blocked by treatment with free radical scavengers, suggesting that a defect in the metabolism of reactive oxygen species is the trigger for apoptosis. In Parkinson’s disease, the death of dopaminergic neurons in the substantia nigra was demonstrated to occur through apoptosis and may be obstructed by delivery of glial-derived neurotrophic factor. Alzheimer’s disease is associated with the progressive accumulation of ?-amyloid protein which is the fundamental component of neural plaques. The ?-amyloid peptide can cause neurons to undergo apoptosis in vitro research studies. �

 

Inherited Metabolic Disease

 

Furthermore, few data suggest that the acute encephalopathy associated with maple syrup urine disease is because of the induction of apoptosis by an accumulating metabolite of leucine, ?-keto isocaproic acid. This compound is a potent inducer of apoptosis in central nervous system glial cells and the result is significantly enhanced in the presence of leucine. Phenylalanine and leucine do not induce apoptosis in this system, suggesting that this result is ultimately unique. �

 

There are two ways in which a cell can die, necrosis and apoptosis. While necrosis occurs due to an external factor which harms the cell, apoptosis follows a controlled, predictable routine. Apoptosis is generally known as programmed cell death. Apoptosis, or programmed cell death, has many fundamental functions in the developing structures of the human body, however, research studies have demonstrated that abnormal apoptosis can be associated with the development of a variety of neurological diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The purpose of the article above is to discuss the process of apoptosis, or cell death, in neurodegenerative diseases. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

What are Brain Disorders?

What are Brain Disorders?

The human brain is the human body’s control center. It is a fundamental structure in the nervous system, which also includes the spinal cord and a system of nerves and neurons. The nervous system controls every structure and function in the human body. When the brain is damaged, it can ultimately affect the function of the nervous system, including memory, sensation, and even personality. Brain disorders include any health issues which affect the brain. This includes health issues due to:

 

  • genetics
  • illness
  • trauma or injury

 

What are the Different Types of Brain Disorders?

 

There is a wide array of different brain disorders which can vary tremendously in symptoms and grade of severity. Below, we will demonstrate the different types of brain disorders and discuss several of the most common types of brain disorders. �

 

Brain Injuries

 

Brain injuries are generally caused by blunt trauma or injury. Trauma or injury can damage brain tissue, neurons, and nerves. This damage affects the brain’s capacity to communicate with the rest of the human body. Several brain injuries include:

 

  • hematomas
  • blood clots
  • contusions or bruising of brain tissue
  • cerebral edema or swelling inside the skull
  • concussions
  • strokes

 

Common symptoms of brain injuries include:

 

  • vomiting
  • nausea
  • speech difficulty
  • bleeding from the ear
  • numbness
  • paralysis
  • memory loss
  • problems with concentration

 

Furthermore, other common symptoms you may develop include:

 

  • high blood pressure
  • low heart rate
  • pupil dilation
  • irregular breathing

 

Depending on the type of brain injury, treatment may include medication, rehabilitation, or brain surgery. Approximately half of the people with acute brain injuries require surgery to remove or repair damaged tissue and to relieve stress. Individuals with mild brain injuries may not require any treatment past medication. Many people with brain injuries may also require:

 

  • physical therapy
  • speech and language therapy
  • psychiatry

 

Brain Tumors

 

Occasionally, brain tumors can develop and they can become quite dangerous. These are known as primary brain tumors. In other instances, cancer from other regions of the body can spread into the brain. These are known as secondary or metastatic brain tumors. Brain tumors may be categorized as either malignant (cancerous) or benign (noncancerous). Healthcare professionals also categorize brain tumors as grades 1, 2, 3, or 4. Higher numbers indicate more severe cancers. �

 

The main cause of the majority of brain tumors is largely unknown. They can occur in people of all age. Symptoms of brain cancers generally depend on the size and location of the tumor. The most common symptoms of brain tumors include:

 

  • headaches
  • seizures
  • tingling sensations or numbness in the arms or legs
  • nausea
  • vomiting
  • changes in personality
  • difficulty with movement or balance
  • changes in hearing, speech, or vision

 

The type of treatment you’ll receive for the brain tumors depends on a variety of different factors, such as the size of the brain tumor, your age, and your overall health and wellness. The main types of treatment for brain tumors include:

 

  • chemotherapy
  • radiation therapy
  • surgery

 

Neurodegenerative Diseases

 

Neurodegenerative disorders cause the brain and the nerves to gradually deteriorate as people age. They can affect an individual’s personality and cause confusion. They are also able to destroy the brain’s tissue and nerves. Brain disorders like Alzheimer’s disease may develop over time with age. It can slowly impair memory and thought processes. Other diseases, such as Tay-Sachs disease are genetic and can develop at any age. Common neurodegenerative diseases include:

 

  • Huntington’s disease
  • ALS (amyotrophic lateral sclerosis), or Lou Gehrig’s disease
  • Parkinson’s disease
  • all types of dementia

 

Several of the most common symptoms of neurodegenerative diseases include:

 

  • Memory loss
  • forgetfulness
  • apathy
  • anxiety
  • agitation
  • a loss of inhibition
  • mood changes

 

Neurodegenerative diseases can ultimately cause irreversible damage and symptoms generally have a tendency of becoming worse as the disease progresses. New symptoms can also continue to develop over time. Unfortunately, there’s no treatment for neurodegenerative diseases, however, treatment can help improve symptoms. The treatment goal for these health issues is to reduce symptoms and maintain quality of life. Treatment often involves the use of medications to control symptoms. �

 

Mental Disorders

 

Mental disorders, or mental illnesses, are a wide variety of health issues which affect behavior patterns. Much like the brain disorders previously mentioned, symptoms can also vary. Several of the most commonly diagnosed mental disorders are:

 

  • depression
  • anxiety
  • bipolar disorder
  • post-traumatic stress disorder (PTSD)
  • schizophrenia

 

The symptoms of mental disorders can vary based on the health issue. Different people can experience exactly the same mental disorders differently. Make sure to speak with a healthcare professional if you notice any changes in your behavior, thought patterns, or mood. The two major types of treatments for mental disorders are medication and psychotherapy. Different treatments work better for different health issues. Many individuals find that a combination of both is best. �

 

If you believe that you may have a mental disorder, it’s important to speak to a healthcare professional for diagnosis in order to determine which treatment program is suitable for you. There are many resources available to treat mental disorders. �

 

What are the Risk Factors for Brain Disorders?

 

Brain disorders can affect anyone, however, the risk factors can ultimately vary for different types of brain disorders. Traumatic brain injury is most common in children under 4 years old, young adults between 15 and 25 years old, and adults 65 and older. Brain tumors may affect any individual at any given age. An individual’s risk for developing brain disorders generally depends on the individual’s genetics and their vulnerability to environmental risk factors, such as radiation. �

 

Older age and family history are the most important risk factors for neurodegenerative diseases. Mental disorders are extremely common. About 1 in 5 American adults have experienced a mental health issue. Your risk may be greater if you:

 

  • have a family history of mental illness
  • have or have had traumatic or stressful life experiences
  • have a history of misusing drugs or alcohol
  • have or have experienced a traumatic brain injury

 

There are a variety of treatment approaches which can help improve brain disorders. The outlook for people with brain disorders depends on the type and severity of the brain disorder. Several of these health issues can be easily treated with the utilization of medication and other therapy methods and techniques. Other brain disorders, such as neurodegenerative diseases and several types of traumatic brain injuries have no cure, however, treatment approaches can help improve symptoms. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The purpose of the article above is to discuss the different types of brain disorders, including neurodegenerative diseases. Neurological diseases are associated with the brain, the spine, and the nerves. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �

 

Curated by Dr. Alex Jimenez �

 


 

Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 


 

Formulas for Methylation Support

 

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.