Back Clinic Chiropractic. This is a form of alternative treatment that focuses on the diagnosis and treatment of various musculoskeletal injuries and conditions, especially those associated with the spine. Dr. Alex Jimenez discusses how spinal adjustments and manual manipulations regularly can greatly help both improve and eliminate many symptoms that could be causing discomfort to the individual. Chiropractors believe among the main reasons for pain and disease are the vertebrae’s misalignment in the spinal column (this is known as a chiropractic subluxation).
Through the usage of manual detection (or palpation), carefully applied pressure, massage, and manual manipulation of the vertebrae and joints (called adjustments), chiropractors can alleviate pressure and irritation on the nerves, restore joint mobility, and help return the body’s homeostasis. From subluxations, or spinal misalignments, to sciatica, a set of symptoms along the sciatic nerve caused by nerve impingement, chiropractic care can gradually restore the individual’s natural state of being. Dr. Jimenez compiles a group of concepts on chiropractic to best educate individuals on the variety of injuries and conditions affecting the human body.
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. �
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
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
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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. �
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There are those that can predict approaching storms, and weather change based on the way, their joints behave.
Similarly, individuals with chronic back pain can at times sense a change in how they feel when the weather shifts.
The connection between weather and back pain is not fully understood but here are a few beliefs on why people feel pain based on the season/weather.
There is not a great deal of research on weather’s effects on spinal conditions. said Dr. Alexander Jimenez, D.C. in El Paso, Texas.
Some spinal conditions have been shown to have a clear link to cold weather. An example is sciatica patients that would experience worsened pain when the weather would shift.
Chiropractor Alexander Jimenez breaks down how weather can affect back pain and explains six ways to help weather-related back pain.
Weather and Osteoarthritis
Dr. Jimenez talks of a study that examined joint pain differencesbetween older people with osteoarthritis that were weather-sensitive versus those who also had osteoarthritis but were not weather-sensitive.
More than two-thirds said weather affected their osteoarthritis pain
Researchers found that weather sensitivity and pain:
More prevalent among women
People with anxiety conditions
Weather and season change alters how we feel mentally and emotionally.
That link is definitely true between depression and back pain.
Dr. Jimenez sees the shift in spine health from the hot summer months into the cold ones and that is when the health problems peak.
Winter brings cloudier weather, and that increasesmelatonin from the brain, which causes drowsiness and less energy.
Sunlight increases serotonin, which causes feelings of happiness.
Cold, dark, winter weather can deplete energy and makes people stay indoors. This is not good because being outside, involved in activity and exercise definitely helps with joint pain.
Staying inside and not moving will worsen pain and possibly lead to severe conditions.
When the seasons begin to change, it also brings to realization the holiday season, which can cause all kinds of:
Anxiety
Stress
Tension
The holiday season can cause major stress, and the changes in weather are a reminder of that upcoming stress.
Theories
A common theory suggests that when the temperature drops it affects the viscosity of the synovial fluid in the joints.
This could be one of the reasons why people with spinal joint pain experience flare-ups during the cold shift.
Dr. Jimenez says that the structures within your:
Joints
Tendons
Ligaments
Muscles
Connective tissues
All have different densities and react differently to temperature changes.
In the cold, some connective tissues are looser than others.
So those that are tighter take longer to warm up, and if not then there is a perfect set-up for joint dysfunction.
Another theory is that barometric pressure is what causes the pain. This theory supports people with joint pain that can tell when it�s about to rain.
Some rheumatologists believe the joint capsule and tissues around the joint are like a balloon.
The barometric pressure squeezes this balloon, causing the balloon to expand/inflammation that causes pain.
Moving to Warmer Climate
Mental
Emotional
Physical
Factors play into how pain affects the individual and moving to a sunny place is not necessarily the answer.
Dr. Jimenez says that warmer climates have been thought to be healthier for various conditions.
In a sunny climate, one is likely to be in the sun, being active physically/mentally,� getting plenty of vitamin D, which is good for bones and joints and makes for a good mood all around.
But moving to a warm climate isn�t always an option, so lifestyle changes can do the trick.
Clinical treatments, like infrared sauna, can bring�the sun’s benefits during dark winter days.
People with chronic pain have said they feel pain-free and relaxed after sitting in an infrared sauna.
An infrared sauna does not give off ultraviolet rays, but healthy light.
The light penetrates into the tissues, warms the body, and makes the connective tissue stretchier and looser, which moves easier and doesn’t hurt.
6 Tips
There is no need to move to a sunny climate.
Dr. Jimenez says you can minimize the weather�s effects with these tips:
Diet
Dr. Jimenez recommends reducing consumption of inflammation-inducing foods like:
Red meats
Fried foods
Sugars
Processed starches
Quitting smoking tobacco is essential for finding pain relief.
Proper Hydration
Alcoholic beverages dehydrate and can worsen depression and anxiety.
Dr. Jimenez says drinking plenty of water is important for the spine, and is often overlooked by the senior community.
Older adults don’t have an active thirst like a young person, and can, therefore, dehydrate rapidly.�
Stay Warm
Layer clothing or keep the house warm.
Keep a humidifier running with the heater to prevent respiratory problems caused by the dry heat.
Get Into The Sun Regularly
Natural light helps wards off depression, and it improves productivity in the workplace
Exercise
Physical activity plays a huge part in particularly with low back conditions, walking, which he said engages the postural muscles in the spine.
Dr. Jimenez personally sees the benefits of this: When I�m working out, I don�t feel my hip pain. And I continue because I know that I’m strengthening my body for the better, especially since I help others with their pain.
Hobbies Can Help
A hobby creates a diversion from the pain and releases endorphins, the body’s natural painkillers.
A hobby allows you to focus on something else besides the pain.
Depression & Chronic pain | El Paso, Tx
Chronic pain caused by accidents and/or aggravated conditions can often be one of the primary reasons for depression in patients. When painful symptoms induce patients to struggle with their everyday physical activities, their mental health can be tremendously influenced. Chiropractic care utilizes spinal adjustments and manual manipulations which could help restore the initial integrity of the backbone. Patients describe how chiropractic care has helped them recover their well-being and they highly recommend Dr. Alex Jimenez, doctor of chiropractic, as the non-surgical choice for chronic pain and depression, one of a variety of other common health issues.
NCBI Resources
Back pain can be debilitating, causing immobility, inflexibility, and have a significant impact on a person�s quality of life. It can make even the most mundane daily activities extremely difficult � and even excruciating. Building the muscles that make up your core (abdominals and back) can help support your spine and reduce back pain. In many cases, strengthening these muscles can assist a patient to avoid medication with its unpleasant side effects and even avoid surgery. With just a few smart moves you can significantly decrease your�back pain, increase your mobility, and take back your life.
Often referred to as C1-C7, with the “C” indicating cervical, and the numbers 1-7 indicate the level.
C1 is closest to the skull
C7 is closest to the thoracic chest/rib cage area
The cervical spine is particularly susceptible to degenerative problems because:
Highly mobile with a broad range of motion
Supports the skull
Neck anatomy is complex
Many degenerative problems, including osteophytes or bone spurs, can develop.
Neck Pain Symptoms
Several symptoms can occur and indicate the presence of a degenerative condition:
Neck pain
Pain around the back of the shoulder area
Arm pain, numbness, or weakness
Difficulty with hand dexterity or walking
Conditions That Affect the Neck
The degenerative process begins in any of the joints in the spine, but over time it can cause changes in the other joints.
An example is an intervertebral disc�where:
The disc narrows and the normal movement becomes altered, and the adjacent joints are subjected to force and pressure, which can lead to degenerative arthritis joint inflammation.
Spondylosis or spinal osteoarthritis causing pain in the neck is common. The pain can radiate, or spread, into the shoulder/s or down the arm/s. Arm pain or weakness caused by a bone spur compressing a spinal nerve root can also occur.
Diagnosing Cervical Spine Conditions
Once examined one or more symptoms are likely to be present.
The doctor will ask the patient questions to learn the history of the patient.
A thorough evaluation of the patient will be conducted, including tests to identify the cause of pain and symptoms.
A neurologic examination is performed to rule out neurological disorders
Shoulder examination will also be done to ensure that the symptoms originate from the neck
Diagnostic tests
X-rays for:
Narrow intervertebral disc space
Anterior osteophytes or bone spurs
Spondylosis (ie, arthritis) of the facet joints
Osteophytes created from the uncovertebral joints
CT Scans or computed tomography can show bone changes associated with degenerative spondylosis. Osteophytes can be observed and evaluated.
CT does not provide an optimal evaluation but can sometimes show disc herniations.
MRI magnetic resonance imaging is a powerful tool for cervical spondylosis.
MRI can help doctors identify:
Disc herniation
Osteophytes
Joint arthrosis a type of osteoarthritis
MRI is best for soft disc herniation/s.
Myelogram/CT can be utilized in complex cases that involve multi-level spinal diseases.
It is very useful in delineating bone spurs from safe disc herniations.
Discography is used diagnostically when viewing the lumbar/low back and thoracic/mid-back spine, but using it in cervical spine imagery is debated among doctors.
Treatment Options
After the tests have been performed, a custom treatment plan is created.
Nonsurgical Neck Pain Treatment
Nonsurgical treatment of cervical degenerative disease has been proven to provide excellent results in over 85% of patients.
A multi-disciplinary approach:
Immobilization of the neck�to reduce motion can be beneficial during acute episodes of pain.
Physical therapy (PT) and Chiropracticcan be useful to decrease muscle spasms and return motion.
Non-surgical treatment provides positive long-term pain and symptom relief.
Surgery
A surgeon is likely to consider surgery for a disorder if one or more of the following criteria are met:
Nonsurgical care has been tried and has not worked
Spinal cord dysfunction
Arm pain or weakness (neurological symptoms) that do not go away
Depending on the diagnosis, surgical procedures can vary:
One type of surgery is the removal of the bone spur(s)
Cervical spinal fusion that joins two or more vertebrae
But the surgical procedure is based on the way you the patient wants to go, the diagnosis, general health, and what the spine surgeon recommends.
The surgeon will explain the recommended procedure to you clearly.
Most of the time the preferred approach is anterior or from the front interbody fusion.
A cervical plate could be placed over the interbody device or graft to stabilize the neck. This can avoid the need for a brace after.
A posterior approach from the back of the spine is considered when a disc has herniated laterally or to the side.
Things You Can Do
Cervical spine disorders can be diagnosed�and treated more accurately with today’s advancing technology.
With the guidance and treatment of an expert medical team, patients can expect to see a definite improvement in their condition and symptoms.
El Paso, TX Neck Pain Chiropractic Treatment
Sandra Rubio discusses the symptoms, causes, and treatments of neck pain. Headaches, migraines, dizziness, confusion, and weakness in the upper extremities are a few of the typical symptoms. Trauma from an accident, such as that from an automobile accident or a sports injury, or an aggravated illness because of improper posture can commonly cause neck pain and other ailments. Dr. Alex Jimenez uses spinal alterations and manual manipulations, one of other chiropractic treatment techniques like deep-tissue massage, to reestablish the alignment of the cervical spine and improve neck pain. Chiropractic care with Dr. Alex Jimenez is your non-surgical choice for restoring general patient well-being.
Neck pain is a frequent health issue, with roughly two-thirds of the people being influenced by neck pain at any time throughout their lifetimes. Numerous other health issues can cause pain arising in the upper back, or the spine. Neck pain can result emanating from the vertebrae, or because of muscular tightness in both the neck and the upper back. Joint disruption in the neck causes migraines, and headache, as does joint disturbance at the trunk, or can generate a variety of other symptoms. Neck pain affects about 5 percent of the worldwide population as of 2010, based on figures.
NCBI Resources
A chiropractor evaluates the spine as a whole because other regions of the�neck (cervical), mid-back (thoracic) and low back (lumbar)�can be affected as well. Along with treating the spine as a whole, chiropractic medicine treats the entire person and not just a specific symptom/s. Chiropractors may�educate on nutrition, stress management, and lifestyle goals in addition to treating neck pain.
When compared to other central nervous system (CNS) health issues, chronic neurodegenerative diseases can be far more complicated. Foremostly, because the compromised mitochondrial function has been demonstrated in many neurodegenerative diseases, the resulting problems in energy sources are not as severe as the energy collapse in ischemic stroke. Therefore, if excitotoxicity contributes to neurodegeneration, a different time of chronic excitotoxicity needs to be assumed. In the following article, we will outline what is known about the pathways that may cause excitotoxicity in neurodegenerative diseases. We will specifically discuss that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. �
Huntington’s Disease
Huntington’s disease (HD) is as an inherited, fatal neurodegenerative disease which is caused by a trinucleotide (CAG) repeat expansion in the coding region of the huntingtin (htt) gene which is associated with the degeneration of the GABAergic medium-sized spiny neurons (MSN) in the striatum, although other brain regions can also ultimately be affected as the health issue progresses. HD is identified as a movement disorder with co-morbid cognitive and psychiatric symptomatology. Both mutant htt RNA together with the encoded protein which includes a polyglutamine repeat expansion is believed to cause the complicated changes in cellular metabolism which occurs in mitochondrial dysfunction and oxidative stress. �
Early research study findings which demonstrated that excitotoxicity may play a fundamental role in HD were based upon the observation that an injection of their KYN metabolite and NMDA receptor agonist QUIN, in addition to L-glutamate and kainate, in the striatum of rats caused neuronal degeneration. Another research study determined that QUIN, as compared to NMDA and kainate, causes selective degeneration of the MSNs instead of neuronal death, which tremendously resembles the pathology of HD. Moreover, NMDA receptors have been shown to be hyperactive and striatal neurons from different HD mouse models, such as a yeast artificial chromosome (YAC) which leads to over-expression of full-length htt with elongated polyglutamine repeats as well as R6/2 mice over-expressing htt exon 1 with elongated polyglutamine repeats in addition to in knock-in mice with greater CAG repeats inserted from the mouse htt gene, were demonstrated to be sensitized to excitotoxicity in vitro. Furthermore, in vivo, a sensitization to an excitotoxin injection into the striatum was only demonstrated in the transgenic YAC model of HD, whereas mice overexpressing mutant htt exon 1, R6/1 and R6/2 mice, or N171-82Q mice overexpressing mutant exon 1 and components of exon 2 or the so-called “shortstop” mouse expressing human N-terminal htt encoded by exon 1 and 2 with a 128 CAG repeat below the htt promoter, produced somewhat of a resistance to striatal excitotoxin injection during the aging process. This neuroprotection isn’t necessarily for NMDA receptor agonists, however, it can help different neurotoxic insults and may be an adaptive response to cellular stress. �
Rat MSN release increased levels of NR2A- and NR2B-containing NMDA receptors compared to interneurons in the striatum. NR1 and NR2B mRNA expression in the neostriatum of HD patients has been demonstrated to considerably decrease which is associated with the loss of these neurons. In addition, NMDA receptor-mediated pathways in MSN were determined to be tremendously sensitive to the NR2B-specific inhibitor ifenprodil. In HEK293 cells, overexpression of mutant htt increased NMDA receptor-mediated pathways and aggravated NMDA-induced cell release only when NR2B- but not when NR2A-containing NMDA receptors were co-expressed. One possible explanation for the increase in NR2B-containing NMDA receptor expression from HD models is that an extended polyglutamine repeat in htt decreases its connection to PSD95, a postsynaptic density protein included in NMDA and kainate receptor clustering, ultimately causing a greater response of PSD95 together with the NR2B subunit. Recently, research study findings suggest that not only does the subunit composition but also the localization of NMDA receptors may play a fundamental role in the NMDA receptor activity. Another research study showed that in severe striatal slice preparations from YAC transgenic mice utilizing 128 CAG repeats, extrasynaptic NMDA receptors, especially those with NR2B, are considerably increased compared to pieces from wild-type mice and YAC mice expressing htt with 18 CAG repeats. As expected from in vitro research studies, this change was associated with decreased CREB phosphorylation. The increased percentage of NR2B-containing extrasynaptic NMDA receptors was demonstrated to be associated with increased extrasynaptic localization of PSD95. One pathway which may cause the sensitization to excitotoxic stimulation downstream of the activation of extrasynaptic NMDA receptors was identified as activation of p38 MAPK. Taken multilayered evidence suggests that mutant htt results in sensitization of MSN into glutamate excitotoxicity through the redistribution of NMDA receptors from subunits to extrasynaptic sites. �
The activation of extrasynaptic NMDA receptors in acute striatal brain slices can be effectively shown in YAC mice utilizing 128 CAG repeats through spillover of synaptic glutamate by restricting EAATs. As a result, it may be determined that decreased EAAT expression may increase the activation of NMDA receptors. Surprisingly, within situ-hybridization, research studies discovered a decrease in astrocytic EAAT2 mRNA expression in the neostriatum of all HD patients. As compared to wild-type mice, however, no changes in protein expression were found to be decreased in synaptosomes of YAC mice overexpressing human htt utilizing 128 CAG repeats. The researchers determined that a decrease in EAAT2 activity from the YAC model of HD was caused by decreased palmitoylation of the transporter. In R6/2 mice, others discovered decreased EAAT2 mRNA and protein expression associated with decreased EAAT2 in synaptosomes or acute cortico-striatal pieces. However, extracellular striatal glutamate concentrations have been shown to be similar to those of wild-type control mice and a decreased glutamate clearance capability in the R6/2 mice demonstrated by therapy with EAAT inhibitors or glutamate. A putative explanation for this finding could be a decrease in glutamate release through system x?c and in xCT, the subunit of system x?c which has been demonstrated at the striatum of R6/2 mice in the mRNA and protein levels. �
As previously mentioned, the injection of the KYN metabolite QUIN in supraphysiological concentrations was utilized as an early animal model of HD. This caused further research studies of KYN metabolism in HD. Surprisingly, the QUIN precursor 3HK aggravates neurodegeneration from the QUIN HD version while KYNA is protective. Research studies discovered that in early-stage HD, compared to control and end-stage HD, neostriatal 3HK and QUIN concentrations were considerably upregulated. Another research study discovered that KYNA levels decreased in autopsied HD striata with the CSF of HD patients when compared with controls. The first enzyme of this KYN pathway, IDO, is triggered from the striatum of both YAC mice with 128 CAG repeats. Mice deficient in IDO are less sensitive to intrastriatal QUIN injection. Evaluation of KYN metabolites from three different mouse models of HD, R6/2 mice, YAC128 mice as well as HdhQ92 and HdhQ111 knock-in mice in various brain regions, suggested age-dependent activation of their KYN pathway. However, the detailed pattern of metabolite changes was different among the versions with increased 3HK in cortex, striatum, and cerebellum in R6/2 mice whereas mice expressing full-size mutant htt demonstrated an extra cortical and striatal upregulation of QUIN. Moreover, treatment of R6/2 mice with a non-blood brain barrier permeable KMO inhibitor, JM6, which indirectly improved cerebral extracellular KYNA concentrations by 50 percent, has been associated with a decrease in extracellular cerebral L-glutamate, decreased neurodegeneration and prolonged survival. Further research studies are still required for further evidence. �
Taken collectively, the research studies support the view that in HD there is a redistribution of both NMDA receptors, especially those containing NR2B, which can activate signaling pathways which boost neurodegeneration, as shown in Figure 5. There is not any evidence that cerebral L-glutamate levels are grossly increased in HD. This might be explained by the fact that even though EAAT2 and KYNA may be downregulated, there is also a downregulation of system x?c action. As only very high levels of QUIN activated NMDA receptors, this KYN metabolite is unlikely to contribute to the excitotoxic load. �
In many research studies, evidence and outcome measures have demonstrated that glutamate dysregulation and excitotoxicity in many neurological diseases, including AD, HD, and ALS, ultimately lead to neurodegeneration and a variery of symptoms associated with the health issues. The purpose of the following article is to discuss and demonstrate the role that glutamate dysregulation and excitotoxicity plays on neurodegenerative diseases. The mechanisms for excitotoxicity are different for every health issue. – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Metabolic Assessment Form
[wp-embedder-pack width=”100%” height=”1050px” download=”all” download-text=”” attachment_id=”72423″ /] � 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. �
In the article above, we outlined what is known about the pathways which may cause excitotoxicity in neurodegenerative diseases. We also discussed that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. 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 �
References
Lewerenz, Jan, and Pamela Maher. �Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?� Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.
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
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�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.
�
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.
Hormone deficiencies and imbalances are more common than one might originally think. Research suggests that “nearly half of the women in the United States have experienced a hormone imbalance” (Grinta, 1) . However, hormone imbalance does not just affect women, “as nearly 35% of males in their seventh decade have lower testosterone levels than younger men”. (McBride, 2)��An imbalance in hormones can cause an array of symptoms and ultimately affect an individuals day to day life.�
Symptoms�
The symptoms of hormone deficiency might not be as obvious as one could imagine. Some symptoms are small and could be brushed off as stress or lack of sleep, but it is important to look at the symptoms for what they really are. “In women, low estrogen can contribute to:
mood swings
hot flashes
headaches
depression
trouble concentrating
fatigue
irregular or absent periods
increased UTI’s “
(Swns, 3)�
In men, some of the symptoms are similar to those in women, but also include:
decreased bone mass
sleep disturbances
decreased motivations
increased body fat
decreased muscle mass
hair loss
libido
(Wallace, 4)
Solutions�
If these symptoms are affecting an individual’s lifestyle, there are multiple steps that can be taken to diagnose the problem and ultimately reduce symptoms. In today’s medical world, practitioners are able to use integrative techniques towards functional medicine, focusing on the biochemical level. If a patient is seeking solutions, the first step taken is an extensive questionnaire. This allows the doctor to pinpoint the exact symptoms, issues, and gives an insider look as to what direction to head towards first.
An example of the questions asked are as follows:
Once the questionnaire is completed and reviewed, a lab test is needed in order to confirm and view the exact levels the hormones are at. D.U.T.C.H ( Dried Urine Test for Comprehensive Hormones) provides one of the most accurate results. To gain more insight on D.U.T.C.H and how it works, please see last week’s article, linked here.
Testing & Conclusions
Filling out the questionnaire�essentially allows the practitioner to score and rate the severity of the issues. Adding the D.U.T.C.H results to the questionnaire gives the practitioner a factual level and complete understanding of their patient’s sex and adrenal hormones and metabolites.
This further allows the practitioner to diagnose (if necessary) and suggest nutraceuticals to help the patient’s hormone levels return to normal and minimize symptoms. There are many factors and systems involved when it comes to treating hormones and having tests completed that reflect the numbers that need to be adjusted is necessary. A hormone imbalance can easily take charge of an individual’s life, but now is the time to get these symptoms under control and get back to feeling like you used to!
A great place to start is to find a doctor or healthcare provider who will supply you with a full questionnaire and listen to the symptoms you’re having. This condition is fairly common and can be treated! October is Chiropractor Health Month, and we would love to see you and aid in providing treatment if you are experiencing any of these symptoms. Due to the fact that hormones can be complex and affect different body systems, we take the time to really understand and check all aspects before jumping to a conclusion. – Kenna Vaughn, Senior Health Coach
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 .
Bibliography
(1) Ginta, Daniela. �What Are the Symptoms of Low Estrogen in Women and How Are They Treated.� Healthline, 31 Jan. 2017, www.healthline.com/health/womens-health/low-estrogen-symptoms.
(2) McBride, J Abram, et al. �Testosterone Deficiency in the Aging Male.� Therapeutic Advances in Urology, SAGE Publications, Feb. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4707424/.
(3) Swns. �Nearly Half of Women Have Been Affected by a Hormonal Imbalance.� New York Post, New York Post, 22 Feb. 2019, nypost.com/2019/02/22/nearly-half-of-women-have-been-affected-by-a-hormonal-imbalance/.
(4) Wallace, Ryan, and Kathleen Yoder. �12 Signs of Low Testosterone .� Healthline, 25 Apr. 2019, www.healthline.com/health/low-testosterone/warning-signs.
Many patients with peripheral neuropathy often believe that their painful symptoms are irreversible or permanent. However, Dr. John Coppola and Dr. Valerie Monteiro describe that peripheral neuropathy can be treated by treating the underlying source of the painful symptoms. Several patients discuss their painful peripheral neuropathy symptoms and how these affected their overall quality of life.
Moreover, the patients also discuss how Dr. John Coppola and Dr. Valerie Monteiro helped treat their painful peripheral neuropathy symptoms through the use of a variety of treatment methods and techniques. Dr. Alex Jimenez, doctor of chiropractic in El Paso, TX, can help treat painful symptoms associated with peripheral neuropathy. Dr. Alex Jimenez is the non-surgical choice for chiropractic care and peripheral neuropathy treatment.
Peripheral Neuropathy Recovery Stories | El Paso, TX (2019)
Neuropathy is a medical term used to describe a collection of general diseases or malfunctions which affect the nerves.
The causes of neuropathy, or nerve damage, can vary among individuals and these may be caused by different:
Diseases
Injuries
Infections
Vitamin deficiencies
Neuropathy can also be classified according to the location of the nerves being affected and according to the disease-causing it.
Furthermore, depending on which nerves are affected will depend on the symptoms that will manifest.
Peripheral neuropathy is simply referred to as neuropathy, which is a state that happens when the nerves become damaged or injured, oftentimes simply disturbed.
It�s estimated that neuropathy affects roughly 2.4 percent of the general populace and approximately 8 percent of people older than age 55.
Type
Neuropathy can affect any of the three types of peripheral nerves:
Sensory nerves�transmit messages from sensory organs:
Eyes
Nose
Brain
Motor nerves track the movement of the muscles
Autonomic nerves regulate the involuntary body functions
Sometimes, neuropathy will only impact one nerve. This is medically referred to as mononeuropathy and instances of it include:
Ulnar neuropathy affects the elbow
Radial neuropathy affects the arms
Peroneal neuropathy affects the knees
Femoral neuropathy affects the thighs
Cervical neuropathy affects the neck
Sometimes, two or more isolated nerves in separate regions of the body can become damaged, injured or disrupted, resulting in mono neuritis multiplex neuropathy.
Most of the time, multiple peripheral nerves malfunction at the same time, a condition called polyneuropathy.
Cause
Neuropathies are often inherited from birth or they develop later in life.
The most frequent inherited neuropathy is the Charcot-Marie-Tooth disease, which affects 1 in 2,500 people in the USA.
Although healthcare professionals are sometimes not able to pinpoint the exact reason for an acquired neuropathy, medically referred to as idiopathic neuropathy.
There are many known causes for them, including:
Systemic diseases – a systemic disease is one that affects the whole body.
Physical trauma
Infectious diseases
Autoimmune disorders
The most frequent systemic cause behind peripheral neuropathy is diabetes, which can lead to chronically high blood glucose levels that harm nerves.
Other systemic issues can cause neuropathy, including:
Kidney disorders permit high levels of nerve-damaging toxic chemicals to flow in the blood
Toxins from exposure to heavy metals include:
Arsenic
Lead
Mercury
Thallium
Drugs/medications, including anti-cancer medications, anticonvulsants, antivirals, and antibiotics
Chemical imbalances because of liver illnesses.
Hormonal diseases, like hyperthyroidism, which disturbs metabolic processes, and potentially induces cells and body parts to exert pressure on the nerves.
Deficiencies in vitamins, such as E, B1 (thiamine), B6 (pyridoxine), B12, and niacin can be vital for healthy nerves.
Alcohol abuse induces vitamin deficiencies and could harm nerves.
Cancers and tumors can exert damaging pressure on nerve fibers and paths.
Chronic inflammation can damage protective tissues around nerves, which makes them more vulnerable to compression, getting inflamed and swollen.
Blood diseases and blood vessel damage, which may damage or injure nerve tissue by decreasing the available oxygen supply
Symptoms
Depending on the reason and unique to each patient, signs, and symptoms of neuropathy can include:
Symptoms are dependent on autonomic, sensory, or motor nerves or a combination are affected.
Autonomic nerve damage can start a chain reaction of physiological functions like blood pressure or create gastrointestinal problems and issues.
Damage or dysfunction in the sensory nerves may impact sensations and sense of equilibrium or balance, while injury to motor nerves affects movement and reflexes.
When both sensory and motor nerves are involved, the condition is known as sensorimotor polyneuropathy.
Complications
Peripheral�neuropathy�may result in several complications, as a result of disease or its symptoms.
Numbness from the ailment can allow you to be less vulnerable to temperatures and pain, making you more likely to suffer from burns and serious wounds.
The lack of sensations in the feet, for instance, can make you more prone to developing infections from minor traumatic accidents, particularly for diabetics, who heal more slowly than other people, including foot ulcers and gangrene.
Furthermore, muscle atrophy may cause you to develop particular physical disfigurements, such as pes cavus, a condition marked by an abnormally high foot arch, and claw-like deformities in the feet and palms.
Treatment
The first step in neuropathy treatment should be finding the root cause that’s causing the neuropathy.
Treatment of diseases such as:
Diabetes
Guillain-Barre syndrome
Rheumatoid arthritis
Sarcoidosis
Other underlying diseases
Prevents continued nerve damage and in cases heals the damaged nerves.
If you are unaware of any underlying disease that is causing the peripheral neuropathy, make sure to let your doctor know of abnormal symptoms.
Medication
Peripheral neuropathy can be treated with various medications.
The first type used to treat mild symptoms are:
Over-the-counter pain medications
In more severe cases:
Opiates
Narcotic medications
Anti-seizure medications
A doctor may prescribe a lidocaine patch or anti-depressants to relieve symptoms.
Patients should thoroughly discuss�neuropathymedication with a doctor before proceeding.
Chiropractic/Massage/Physical Therapy
Various manual therapies can benefit symptoms in neuropathy treatment.
A therapist or chiropractor will perform various manipulation techniques, and teach exercises and stretches to help improve symptoms combined with increased muscle strength/control.
A therapist may also recommend braces or splints to improve mobility.
Patients should attend all physical therapy sessions to gain maximum benefits.
Acids
Supplements like:
Essential acids called ALA (alpha-Lipoic acid)
GLA (gamma-linolenic acid) and omega-3 fatty acids
These can have a beneficial effect on diabetic peripheral neuropathy.
L-Carnitine
L-carnitine is a substance that the body makes and stores in the:
Liver
Brain
There have been reports that certain diabetics with neuropathy symptoms could regain regular sensation in the limbs when they increased their consumption of carnitine called acetyl-L-carnitine.
Red meat
Peanut butter
Dairy products
Are good dietary sources of this nutrient.
Supplements are also available at health food stores and pharmacies and health/wellness clinics.
Vitamin Supplements
Vitamin deficiencies can result in peripheral neuropathy in some people.
Therefore there needs to be a replenishing of vitamins:
B
B12
E
These can help to decrease symptoms.
Recommended dosages are 300mg daily of vitamin E.
Doses of the different B vitamins differ, but one option for patients is to take a daily B-complex supplement.
Herb Supplements
Herbal remedies are an alternative to explore.
St. John’s Wort, is a herbal supplement that can be taken orally and can reduce the pain.
Topical creams that have capsaicin, which is an anti-inflammatory found in chili peppers, can reduce the burning sensation.
While every type of neuropathy, such as diabetic neuropathy or autoimmune disease-associated neuropathy, develops its own unique group of symptoms, many patients will often report common complaints. Individuals with neuropathy generally describe their pain as stabbing, burning or tingling.
If you experience unusual or abnormal tingling or burning sensations, weakness and/or pain in your hands and feet, it�s essential to seek immediate medical attention in order to receive a proper diagnosis of the cause of your specific signs and symptoms. Early diagnosis may help prevent further nerve injury. Visit www.neuropathycure.org.
When compared to other central nervous system (CNS) health issues, chronic neurodegenerative diseases can be far more complicated. Foremostly, because the compromised mitochondrial function has been demonstrated in many neurodegenerative diseases, the resulting problems in energy sources are not as severe as the energy collapse in ischemic stroke. Therefore, if excitotoxicity contributes to neurodegeneration, a different time of chronic excitotoxicity needs to be assumed. In the following article, we will outline what is known about the pathways that may cause excitotoxicity in neurodegenerative diseases. We will specifically discuss that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. �
Alzheimer’s Disease
Alzheimer’s disease (AD) is one of the main causes of dementia among older adults in the United States. Neuropathologically, AD is characterized as neurodegeneration with extracellular senile plaques made up of ? amyloid (A?) and intraneuronal neurofibrillary tangles of aggregated tau, which initially appear in the hippocampus than then spread as the health issue progresses. Prominent microglial cell activation can also be associated with AD. Hereditary types of AD occur due to mutations in the A? precursor protein, A?PP, or in the presenilins, which are part of the multi-protein complex involved in A? generation. The pathophysiology of AD is complicated and a variety of pathways are included in the synaptic and the cellular degeneration in AD, such as abnormalities in signaling pathways through glycogen synthase kinase-3 beta or mitogen-activated protein kinases, cell cycle re-entry, oxidative stress, or decreased transport of trophic factors and adrenal dysregulation. However, evidence suggests that L-glutamate dysregulation plays a critical role in Alzheimer’s disease. �
Research studies demonstrated that primary neurons from transgenic mice overexpressing mutant presenilin are far more sensitive to excitotoxic stimulation in vitro. In vitro, aggregated A? increases both NMDA and kainate receptor-mediated L-glutamate toxicity, perhaps by interrupting neuronal calcium homeostasis. Others have demonstrated that A? can increase neuronal excitability by changing the capacity of glycogen synthase kinase 3? inhibition to decrease NMDA receptor-mediated pathways. Soluble A? oligomers were demonstrated to cause L-glutamate release from astrocytes resulting in dendritic spine loss through over-activation of extrasynaptic NMDA receptors. Moreover, extracellular L-glutamate concentrations were demonstrated to increase in a triple transgenic mouse model of AD, in which a 3-month treatment with the NMDA receptor inhibitor ultimately affected synapse loss. However, further research studies are still required. �
Numerous mouse research studies have demonstrated the consequences of AD-like pathology on EAAT expression and/or function. In acute hippocampal slice preparations, A? was shown to interrupt the clearance of synaptically released L-glutamate by diminishing membrane insertion of EAAT2, a result perhaps mediated by oxidative stress. In aged A?PP23 mice, research studies revealed the downregulation of EAAT2 expression in the frontal cortex and hippocampus, which in the frontal cortex was associated with an increase in xCT expression. These changes were associated with a strong tendency toward improved extracellular L-glutamate amounts as measured by microdialysis. In triple transgenic AD mice expressing the amyloid precursor protein mutations K670N and M671L, the presenilin 1 mutation M146V and the tau P301L mutation, a strong and age-dependent decrease of EAAT2 expression was demonstrated. Restoration of EAAT2 activity in the AD mice following treatment with all the ?-lactam antibiotic Cef was associated with a decrease in cognitive impairment and reduced tau pathology. In human AD brains, decreased expression of EAAT2 protein and a decrease in EAAT action was determined. However,� this outcome measure could not be replicated by other researchers. On the transcriptome level, research studies discovered exon-skipping splice variations of EAAT2 which reduce glutamate transport activity to be upregulated in human AD brains. From the CSF, several groups demonstrated an increase in glutamate concentrations in AD patients where other groups demonstrated absolutely no change or even diminished levels of L-glutamate associated with Alzheimer’s disease. �
In vitro, A? causes L-glutamate discharge from primary microglia through the upregulation of program x?c. Others discovered that it also triggered L-glutamate release from astrocytes through the activation of the ?7 nicotinic acetylcholine receptor. Additionally, xCT, the specific subunit of system x?c is upregulated at the region of senile plaques, possibly in microglial cells, in Thy1-APP751 mice (TgAPP) expressing human APP bearing the Swedish (S: KM595/596NL) and London (L: V6421) mutations after A? injection in the hippocampus. Semiquantitative immunoblot evaluations revealed an upregulation of xCT protein expression in the frontal cortex in elderly A?PP23 mice compared to wild-type controls. �
Postmortem research studies show that KYN metabolism affects AD elevated concentrations of KYNA while also discovered in the basal ganglia of both AD sufferers. Utilizing immunohistochemistry, research studies demonstrated immunoreactivity for both IDO and QUIN upregulated in AD brains, particularly in the vicinity of plaques. A? causes IDO expression in human primary macrophages and microglia. Systemic inhibition of KMO ultimately increases brain KYNA levels and ameliorated the phenotype of a mouse model of AD, indicating an upregulation of KYNA may be an endogenous protective reaction, including the IDO inhibitor, coptisine, decreased microglial, astrocytic activation and cognitive impairment in AD mice. �
Taken together, along with many other harmful changes, there is evidence for chronic excitotoxicity in AD which can be driven by numerous variables, including the central sensitization of both NMDA receptors, a decrease in L-glutamate and L-aspartate reuptake capacity and an increase in glutamate release through system x?c, as shown in Figure 4. Although the KYN pathway seems to be upregulated in AD, no specific conclusions can be drawn regarding glutamatergic neurotransmission from the upregulation of the two QUIN which was neurotoxic and neuroprotective KYNA. �
�
In many research studies, evidence and outcome measures have demonstrated that glutamate dysregulation and excitotoxicity in many neurological diseases, including AD, HD, and ALS, ultimately lead to neurodegeneration and a variery of symptoms associated with the health issues. The purpose of the following article is to discuss and demonstrate the role that glutamate dysregulation and excitotoxicity plays on neurodegenerative diseases. The mechanisms for excitotoxicity are different for every health issue. – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight
In the article above, we outlined what is known about the pathways which may cause excitotoxicity in neurodegenerative diseases. We also discussed that in amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Huntington’s disease (HD) as fundamental examples with sufficiently validated animal models in research studies. 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 �
References �
Lewerenz, Jan, and Pamela Maher. �Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?� Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.
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
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�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.
�
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.
IFM's Find A Practitioner tool is the largest referral network in Functional Medicine, created to help patients locate Functional Medicine practitioners anywhere in the world. IFM Certified Practitioners are listed first in the search results, given their extensive education in Functional Medicine
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