Back Clinic Nerve Injury Team. Nerves are fragile and can be damaged by pressure, stretching, or cutting. Injury to a nerve can stop signals to and from the brain, causing muscles not to work properly and losing feeling in the injured area. The nervous system manages a great majority of the body’s functions, from regulating an individual’s breathing to controlling their muscles as well as sensing heat and cold. But, when trauma from an injury or an underlying condition causes nerve injury, an individual’s quality of life may be greatly affected. Dr. Alex Jimenez explains various concepts through his collection of archives revolving around the types of injuries and condition which can cause nerve complications as well as discuss the different form of treatments and solutions to ease nerve pain and restore the individual’s quality of life.
The information herein is not intended to replace a one-on-one relationship with a qualified healthcare professional or licensed physician and is not medical advice. We encourage you to make your own health care decisions based on your research and partnership with a qualified health care professional. Our information scope is limited to chiropractic, musculoskeletal, physical medicines, wellness, sensitive health issues, functional medicine articles, topics, and discussions. We provide and present clinical collaboration with specialists from a wide array of disciplines. Each specialist is governed by their professional scope of practice and their jurisdiction of licensure. We use functional health & wellness protocols to treat and support care for the injuries or disorders of the musculoskeletal system. Our videos, posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate to and support, directly or indirectly, our clinical scope of practice.* Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We provide copies of supporting research studies available to regulatory boards and the public upon request.
We understand that we cover matters that require an additional explanation of how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.
Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may ultimately cause a variety of neurodegenerative diseases and other health issues. Many of the neurodegenerative diseases following TBI include health issues such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). �
The mechanisms underlying the pathogenesis which result in these type of neurodegenerative diseases, however, are still completely misunderstood. Where many of the health issues following TBI have a high incidence, there are currently only several treatment approaches which can help prevent the pathological development of chronic neurological diseases. �
A better understanding of the mechanisms underlying TBI and neurodegenerative diseases is ultimately fundamental to determine the possible connection between these health issues to allow safe and effective diagnosis and treatment. In part 1 of the following article, we will discuss the pathological mechanisms of traumatic brain injury (TBI) and how it’s associated with the development of a variety of neurological diseases and other health issues, including Alzheimer’s disease (AD). �
Pathological Mechanisms of Traumatic Brain Injury
In most instances, TBI is caused by a physical blow to the head during traumatic events, such as falls, automobile accidents, or sports-related accidents, although TBI may also be aggravated by exposure to explosive blasts. TBI can be characterized as mild, moderate, or severe according to the symptoms, such as the length of loss of consciousness and post-traumatic amnesia. Mild TBI (mTBI) is prevalent in the majority of cases, however, it may be difficult to diagnose. This difficulty in diagnosis can be a serious concern as a result of severe consequences like instant impact syndrome or other health issues. �
Damage to the nervous tissue can be characterized as the main injury which happens as a direct effect of a physical blow and secondary injury which happens due to pathophysiological processes subsequent to the traumatic event. The injury process occurs from the rapid acceleration-deceleration of the brain which is believed to harm the brain by causing sheer force within tissue resulting in impact and axonal injury with the cranial wall. These injuries can be contralateral or ipsilateral to the physical blow. In more severe instances, the injury may cause intracranial hypertension and intracranial hemorrhage. This increase in pressure not only damages brain tissue but it also causes potential injury and cerebral hypoperfusion. �
Secondary injury in TBI generally happens several days, weeks, and even months following the traumatic circumstance because of the biochemical changes which occur in the nervous tissue. This harm is often mediated by free radicals and reactive oxygen species (ROS) which develop from ischemia-reperfusion damage, glutamatergic excitotoxicity, or neuroinflammation. After the injury, axonal damage from the sheer force of injury can affect membrane balance. Moreover, uptake of calcium through either membrane disruption or activation of the NMDA and the AMPA receptors by glutamate could ultimately cause mitochondrial dysfunction as well as the overproduction of free radicals and the activation of apoptotic caspase signaling. Following inflammatory processes associated with TBI, such as the activation of microglial cells, can cause oxidative stress through the effects of inflammatory cytokines. These radicals can also cause cellular damage through lipid peroxidation and protein modifications which can overwhelm endogenous antioxidant systems. The secondary products of free radical-mediated lipid peroxidation, such as reactive carbonyl species, can also be electrophilic and can further propagate oxidative damage to biomacromolecules, which can be associated with various neurological diseases. �
Clinical and preclinical research studies have demonstrated the presence of oxidative stress and its byproducts following TBI with both serological and histological methods and techniques. In animal research studies, these products have been demonstrated to continue over a recurrent injury and it may increase following a single traumatic event. Spectroscopic evaluations suggest that the endogenous antioxidants glutathione and ascorbic acid may decrease for 3 to 14 days following the injury. Furthermore, the increase of F2-isoprostane, a lipid peroxidation byproduct, was demonstrated in the cerebrospinal fluid of severe TBI patients with increased levels at 1 day following the injury, however, this was primarily an assessment of alternative treatment and didn’t establish a contrast with healthy controls. Lipid peroxidation products like 4-hydroxynoneal were also found to be elevated in the serum of acute TBI patients needing treatment. Although chronic oxidative stress has not currently been detected following single mild injuries in people, it seems possible that oxidative stress and its associated processes may aggravate or prolong post-concussive symptoms. Given the involvement of oxidative stress in excitotoxicity and reperfusion injury, it’s possible that oxidative stress plays a role in cerebral injury after TBI. �
The pathological mechanisms of secondary TBI are particularly interesting due to the ability to prolong cellular injury beyond the initial traumatic event. Some of these characteristic modifications, such as oxidative stress and excitotoxicity, have also been demonstrated in the pathophysiology of neurodegenerative diseases and other health issues which also suggests a possible pathological mechanistic connection between TBI and neurological diseases. Further research studies of the pathological mechanisms in cerebral diseases and TBI may help determine the factors for neurodegenerative diseases. �
Conclusion
Despite the prevalence of TBI the significant neurological sequelae associated with such injuries, diagnosis, and treatment of TBI remains greatly misunderstood. In addition, the causing factors connected to TBI and neurodegenerative diseases, such as AD, PD, ALS, and CTE, have not been fully determined. Several processes, including oxidative stress and neuroinflammation, have also been found to be common between secondary TBI and several neurodegenerative diseases. In particular, oxidative stress appears to be the key mechanism connecting neuroinflammation and glutamatergic excitotoxicity in both TBI and neurological diseases. It is possible that the oxidative cascade caused by TBI ultimately causes and results in the characteristic pathologies of neurodegenerative diseases through oxidation or carbonylation of essential proteins. �
Due to the high prevalence of TBI and neurodegenerative diseases, the development of new safe and effective treatment approaches for TBI is fundamental. Given the essential role that oxidative stress plays in connecting secondary injury and neurodegeneration, detection of ROS and key byproducts could serve as a method or technique for the diagnosis and treatment of potential cellular damage. Finally, these reactive species may serve as a viable therapeutic target for reducing long-term neurodegenerative disease risk following TBI, helping to reduce the disability and death as well as improve the quality of life of individuals in the United States that suffer from traumatic brain injury (TBI) and other health issues. �
Traumatic brain injury is among one of the most prevalent causes of disability and death among the general population in the United States. According to a variety of research studies, mild, moderate, and severe traumatic brain injury has been associated with neurodegenerative diseases, such as Alzheimer’s disease, as well as a variety of other neurological diseases and health issues. It is fundamental to understand the pathophysiological mechanisms of traumatic brain injury while further research studies are still required to determine the association between TBI and neurodegenerative diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Traumatic brain injury (TBI) is one of the most common causes of disability and death in people. About 1.6 million individuals suffer traumatic brain injuries in the United States every year. TBI can cause a process of injury which may cause a variety of neurodegenerative diseases and health issues, such as Alzheimer’s disease (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
� �
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.
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. �
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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. �
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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. �
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
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.
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. �
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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). �
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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
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.
Low-level laser therapy (LLLT), also known as photobiomodulation, is the use of low-power lasers or light-emitting diodes (LEDs) for treatment purposes. When LLLT is used on the brain, it is known as transcranial LLLT or transcranial photobiomodulation. Many research studies have shown that LLLT can help treat a variety of brain health issues. �
Different from high-intensity surgical lasers, low-powered lasers do not cut or burn tissue. Instead, these lasers stimulate a biological reaction and promote cells to function properly. Moreover, it�s also easy to use LLLT utilizing red and near-infrared light on your own home. In the article below, we will discuss the brain health benefits of low-level laser therapy (LLLT). �
How Low-Level Laser Therapy Works
Research studies show that red and near-infrared light between the wavelengths of 632 nanometers (nm) and 1064 nm can have brain health benefits. For brain cells or neurons, the optimal range for the wavelengths seems to be between 800 nm and 1000 nm as these can penetrate the scalp and skull to reach the brain. Most devices ultimately fall within this range. �
The light given off from these devices stimulate a photochemical response within neurons or brain cells, which can increase the natural healing process and can also cause beneficial changes in their behavior by supporting the mitochondria. The mitochondria are the �powerhouses of the cell,� producing most of the energy in the human body in the form of adenosine-5- triphosphate (ATP). ATP is the cell’s main source of energy. The brain constantly needs to use it to function properly. �
Proper mitochondrial function and ATP production are fundamental for neuroprotection and cognitive enhancement as well as for the prevention and treatment of a variety of neurological diseases. Research studies have shown that transcranial LLLT promotes proper mitochondrial function and considerably improves the production of ATP in the human brain. �
The mitochondria have photoreceptors which absorb the photons from light and turn them into ATP or energy which can be utilized to perform cellular tasks and biological processes. This system is similar to that of plant photosynthesis where sunlight is absorbed by plants and turned into energy for the plants to grow. Furthermore, by stimulating the mitochondria and producing more ATP, LLLT gives brain cells or neurons even more ATP energy to better heal and repair themselves. �
On top of this, low-level laser therapy has also been shown to: �
Decrease free radicals and oxidative stress in the brain
Increase blood flow and circulation, including within the frontal cortex
Reduce pain by supporting the human body�s opioids or natural pain relievers
Increase rate of oxygen consumption in the frontal cortex
Increase serotonin
Many traumatic brain injuries and neurological diseases can be treated with LLLT, including anxiety, depression, post-traumatic stress disorder (PTSD), post-concussion syndrome, stroke, Alzheimer’s disease, and dementia. We will discuss how low-level laser therapy (LLLT) has been shown to help each of the brain health issues, among others, demonstrated below. �
LLLT for Traumatic Brain Injury
Traumatic brain injury (TBI) is a growing brain health issue where approximately 1.7 million people experience some type of TBI in the U.S. every year. Mild TBIs or concussions make up about 75 percent of all traumatic brain injuries. Military personnel frequently experience TBI and many of them often struggle with PTSD, anxiety, and depression. �
Several research studies have shown that patients with chronic mild TBI have experienced improved cognition, memory and sleep with LLLT. One research study also evaluated whether LLLT could help treat 11 patients with chronic mild TBI symptoms. Two patients had cognitive dysfunction and four patients had multiple concussions. �
After 18 LLLT sessions, the patient’s cognition, memory and verbal learning improved. Participants also said that they slept better and had fewer PTSD symptoms. Coworkers, friends, and family also reported improved social, interpersonal, and occupational functioning. In another research study, 10 people with chronic TBI were given 10 LLLT sessions and experienced reduced headaches, cognitive dysfunction, sleep problems, anxiety, depression and irritability. �
Several mice research studies also show that LLLT can prevent cell death and increase neurological performance after TBI. Researchers believe that LLLT improves TBI symptoms because the mitochondria in the brain can become dysfunctional after TBI, resulting in an inadequate supply of ATP. LLLT can support the mitochondria and increase ATP production. �
After traumatic brain injury (TBI) there is also poor blood flow and oxygenation, and increased inflammation and oxidative stress in the brain. This can ultimately cause brain damage, however, LLLT can help treat these brain health issues as well as help increase antioxidants, promote neurogenesis, and relieve chronic symptoms, among other brain health benefits. �
LLLT for Depression and Anxiety
Research studies in both rats and humans have shown that LLLT can improve mood and reduce symptoms of depression. In 2009, researchers took 10 patients with a history of major anxiety and depression, including PTSD and substance abuse, and utilized LLLT for four weeks. At the end of the research study, six of the 10 patients experienced remission of their depression and seven of the 10 patients experienced remission of their anxiety. There were no observable side-effects. �
Several research studies have shown that depression is associated with abnormal blood flow in the frontal cortex of the brain. LLLT increases blood flow and circulation. Other research studies have shown that participants report improved positive emotions and reduced depressive symptoms after LLLT treatment. Participants with TBI also experienced a decrease in anxiety, depression, irritability, and insomnia as well as an overall improvement in quality of life after LLLT. �
LLLT for Alzheimer’s Disease and Dementia
Research studies show that LLLT can boost performance and improve cognitive function, including attention and memory, in animals, young healthy people and elderly people. Preliminary research studies also show that LLLT may ultimately help slow down the progression of Alzheimer�s disease by decreasing a protein in the brain which is associated with dementia. �
The downregulation of brain-derived neurotrophic factor (BDNF) occurs early in the progression of Alzheimer’s disease and dementia. Research studies have shown that LLLT can also help prevent brain cell or neuron loss by upregulating BDNF. �
Researchers have also utilized LLLT in middle-aged mice and discovered that the memory and cognitive performance of the middle-aged mice improved so much that it became similar to that of young mice. The researchers concluded that LLLT should be utilized in cases of general cognitive impairment in elderly people or even for Alzheimer’s disease and dementia. �
Several other research studies have shown that LLLT increases alertness, awareness and sustained attention as well as improves short-term memory and reaction time. Research study participants also made fewer errors during tests. Another research study found that LLLT enhanced cognition by promoting neuroprotection and supporting the mitochondria. �
LLLT for Stroke
Numerous studies also show that LLLT reduces neurological problems and improves behavior in rats and rabbits after stroke. It also increases the growth of new brain cells or neurons, improving their overall recovery. Multiple other research studies also show that LLLT can considerably reduce brain damage and improve recovery outcome measures after a stroke. �
In one research study, researchers utilized LLLT on patients approximately 18 hours after they experienced a stroke. Five days after the stroke, they found considerably greater improvements in the LLLT-treated group. The improvements continued 90 days after the stroke. At the end of the research study, 70 percent of the patients treated with LLLT had successful outcome measures in comparison with only 51 percent of the control subjects in the research study. �
Follow up research studies with over 600 stroke patients found similar brain health benefits associated with low-level laser therapy (LLLT). Researchers believe that the increase in the production of ATP is responsible for the improvements. �
Low-level laser therapy, or LLLT, is a non-invasive treatment approach which utilizes low-power lasers or light-emitting diodes for the treatment of brain health issues and neurological diseases. Many research studies with both animal and human trial have demonstrated that LLLT provides many brain health benefits without harmful side-effects. Healthcare professionals can help improve the symptoms of brain health issues and neurological diseases with a variety of treatment methods and techniques. Proper diagnosis is fundamental for proper treatment. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Low-level laser therapy (LLLT), also known as photobiomodulation, is the use of low-power lasers or light-emitting diodes (LEDs) for treatment purposes. In the article above, we discussed the brain health benefits of low-level laser therapy (LLLT) on a variety of brain health issues and neurological diseases. 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
�
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.
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
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.
The human brain comprises approximately billions of small cells that utilize electrical impulses and chemical signals to communicate with one another and other parts of the human body. These are known as neurons. When neurons stop functioning properly, it can cause various brain disorders, such as Alzheimer’s disease, epilepsy, and even depression.
Researchers developed several treatment methods and techniques of brain stimulation which allow them to control neural activity to understand better and regulate these type of health issues. In conventional treatment methods and techniques of deep brain stimulation, electrical neurostimulators, also known as brain pacemakers, are surgically implanted in the brain.
Researchers also developed non-invasive treatment approaches to stimulate cells found deep within the brain. While several researchers utilize magnetic pulses or sound waves to stimulate neurons, researchers in optogenetics utilize light therapy. Shuo Chen, Ph.D., winner of Science and PINS Prize for Neuromodulation, was recognized for his work in this area.
Dr. Chen demonstrated that near-infrared light, when utilized with certain nanoparticles, allowed the stimulation of neurons deep within the brain, stated Dr. Karl Deisseroth, professor of bioengineering, psychiatry, and behavioral sciences at Stanford University. More research studies are needed to make this a useful process, he said, but Dr. Chen took a key step.
Developing Light-Sensitive Neurons
Dr. Karl Deisseroth, one of the leading pioneers of optogenetics, developed a treatment method or technique in which the brain cells or neurons are genetically engineered to respond to light therapy. Through this method or technique of brain stimulation, researchers transmit fragments of genetic codes from algae and other microbes into the brain cells of mice and other animals. That genetic code ultimately causes neurons to produce light-responsive proteins known as opsins.
When opsin-producing neurons are exposed to specific wavelengths of visible-spectrum light, those brain cells turn on or off. By activating or suppressing the neurons, researchers can learn more about the fundamental role of neurons in brain function and brain disorders. Dr. Karl Deisseroth has also demonstrated the effects of developing light-sensitive neurons.
By developing light-sensitive brain cells, the causal role of cellular activity can be determined in the tissue and the behavior of interest of any species, ranging from memory to mood, stated Dr. Deisseroth. Furthermore, optogenetics brings the unmatched capability for speaking the brain’s natural language regarding cell-type specificity and speed, he added.
Developing Non-Invasive Treatment Approaches
Opsin-producing neurons, however, respond to visible-spectrum light which cant penetrate brain tissue. Therefore, optogenetic stimulation required the insertion of fiber-optic light sources inside the brain to stimulate neurons. Dr. Deisseroth and his colleague Polina Anikeeva, Ph.D., developed the utilization of near-infrared (NIR) light, a non-invasive type of light therapy.
NIR light can ultimately penetrate through the skull and brain tissue without inserting internal light sources inside the brain. However, NIR light also doesn’t trigger a response from opsin-producing neurons. To promote the tissue-penetrating abilities of NIR light therapy, Dr. Karl Deisseroth and Dr. Anikeeva developed a treatment approach known as NIR upconversion, which coats opsin-producing neurons in nanoparticles to convert NIR light into visible-spectrum light.
Dr. Shuo Chen utilized this treatment method and technique, demonstrating for the first time that NIR upconversion optogenetics can ultimately be utilized to control neurons deep in the brains of mice. In addition, Dr. Chen’s research studies utilized this method and technique to stimulate the release of dopamine in a region of the brain believed to play a role in depression.
Overcoming the challenge of optical penetration depth will be the fundamental key to realizing non-invasive remote optogenetics with high clinical translation potential, wrote Dr. Chen in his prizewinning essay on the topic. Our research study utilized a nanomaterial-assisted approach that shifts the existing optogenetic tools into the near-infrared region.
Brain Stimulation for the Human Brain
While researchers continue to research optogenetics in mice and other animals, it hasn’t been utilized to treat brain disorders in humans. Furthermore, more research studies are required to develop and evaluate non-invasive methods of light therapy and non-invasive methods and techniques for transmitting genetic code into brain cells or neurons.
It is too soon to predict which treatment approach will emerge at the forefront of next-generation non-invasive brain stimulation technology, Dr. Chen said in a press release issued by the American Association for the Advancement of Science. However, we believe that a variety of fundamental achievements, such as NIR upconversion optogenetics, are quickly unlocking development pathways and paving the way towards a bright therapeutic future for brain diseases, he continued.
In the meantime, other methods and techniques of non-invasive brain stimulation are also being developed, evaluated, and utilized in humans. For example, transcranial magnetic stimulation (TMS) is a non-invasive treatment approach that utilized magnetic fields to stimulate nerve cells in the brain. The Food & Drug Administration (FDA) has already allowed TMS marketing as a treatment approach for major depression as well as obsessive-compulsive disorder and migraine headaches.
There are also several non-invasive methods and techniques which don’t require the utilization of gene therapies, such as transcranial magnetic and electrical stimulation, which are commonly utilized with human subjects on an experimental, regular basis, stated Ed Boyden, Ph.D., a professor of neurotechnology at the Massachusetts Institute of Technology (MIT).
Members of Boyden”s research study group have also conducted research studies on transcranial electric stimulation (TES), a non-invasive treatment approach to brain stimulation in which electrodes are placed on the scalp. Researchers hope for this method and technique to reach neurons or cells deep within brain tissue with greater precision than TMS.
Although research studies have demonstrated that light therapy can stimulate brain cells or neurons of mice and other animals, urther research studies are required to determine how light therapy treatment methods and techniques can stimulate the human brain. According to these same research studies, light therapy can alter neurons or brain cells which can ultimately cause Alzheimers disease, epilepsy, and other brain diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
The human brain consists of billions of small cells or neurons which communicate with one another and other parts of the human body. When neurons stop functioning properly, it can cause a variety of brain disorders. Researchers have developed a variety of light therapy treatment approaches to help stimulate the brain ultimately. The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues and 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 from the average pain type. The human body will continue sending pain signals to the brain with chronic pain, regardless of the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility, reducing 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 various 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.
According to research studies, transcranial infrared laser stimulation, as well as other types of transcranial lasers, utilized on frontal cortex functions can improve sustained attention and working memory, among other brain functions. Transcranial laser stimulation with low-power density (mW/cm2) and high-energy density (J/cm2) monochromatic light in the near-infrared wavelengths regulates and maintains brain functions and may promote neurotherapeutic effects in a non-destructive and non-thermal manner. Researchers determined through the first controlled research study that transcranial laser stimulation improves human cognitive and emotional brain functions. �
In the field of low-level light/laser therapy or LLLT, developing a model to demonstrate how luminous energy from red-to-near-infrared wavelengths improves bioenergetics has been in development for the last 40 years. Previous LLLT research studies have demonstrated historical a variety of developments, principles and applications on the subject matter. The purpose of the following article is to demonstrate an update on LLLT’s neurochemical mechanisms supporting transcranial laser stimulation for cognitive-enhancing functions. We will describe the effect of LLLT on brain bioenergetics, briefly discussing its bioavailability and dose-response, and its effects on cognitive brain function. Although our focus is on prefrontal-related cognitive functions, LLLT should be able to improve other brain functions. By way of instance, stimulating different brain regions affect different functions associated with sensory and motor systems. �
Transcranial Lasers on Brain Bioenergetics
Near-infrared lasers and light-emitting diodes, or LEDs, affect brain function according to bioenergetics, a mechanism which is fundamentally different than other brain stimulation methods and techniques, such as electric and magnetic stimulation. LLLT has been demonstrated to regulate and maintain the function of neurons in cell cultures, and brain function in animals as well as cognitive and emotional functions in patients and health issues. Photoneuromodulation is associated with the absorption of photons by certain molecules in neurons which activate bioenergetic signaling pathways after being exposed to red-to-near-infrared light. The 600mm to 1150 nm wavelengths provide improved tissue penetration by photons because light is scattered at lower wavelengths and absorbed by water at higher wavelengths. Over 25 years ago, it was demonstrated that molecules which absorb LLLT wavelengths are part of the mitochondrial respiratory enzyme cytochrome oxidase in different oxidation states. Moreover, for red-to-near-infrared light, the main molecular photoacceptor of photon energy is cytochrome oxidase, also known as cytochrome c oxidase or cytochrome a-a3. �
Furthermore, photon energy absorption by cytochrome oxidase is the main neurochemical mechanism of action of LLLT in neurons. The more the enzymatic activity of cytochrome oxidase increases, the more metabolic energy which is developed through mitochondrial oxidative phosphorylation. LLLT provides the brain with metabolic energy in an analogous manner to the conversion of nutrients into metabolic energy with the utilization of light instead of nutrients developing the source for ATP-based metabolic energy. If an effective near-infrared light energy dose is provided, it stimulates brain ATP production and blood flow, ultimately fueling ATP-dependent membrane ion pumps, promoting greater membrane stability and resistance to depolarization, which has been demonstrated to transiently reduce neuronal excitability. Electromagnetic stimulation also directly affects the electrical excitability of neurons, as demonstrated in research studies. �
A long-lasting effect is provided by LLLT’s up-regulating the amount of cytochrome oxidase, which improved neuronal capacity for metabolic energy production which can be utilized to improve cognitive brain functions. In mice and rats, memory has been demonstrated to improve by LLLT and by methylene blue, a drug, which at low doses, provides electrons to cytochrome oxidase. Near-infrared light stimulates mitochondrial respiration by providing photons to cytochrome oxidase because cytochrome oxidase mainly accepts photons from red-to-near-infrared light in neurons. By stimulating cytochrome oxidase activity, transcranial LLLT promotes post-stimulation up-regulation of the amount of cytochrome oxidase in brain mitochondria. LLLT may also improve the conversion of luminous energy into metabolic energy during light exposure as well as the up-regulation of the mitochondrial enzymatic machinery to develop more energy after light exposure. �
Bioavailability and Hormetic Dose-Response by Transcranial Lasers
The most numerous metalloprotein found in nerve tissue is cytochrome oxidase and its absorption wavelengths are often associated with its enzymatic activity and ATP production. Increased LLLT bioavailability to the brain in vivo has been demonstrated in a variety of research studies by exposing brain cytochrome oxidase activity transcranially, resulting in improved extinction memory retention in healthy rats and improved visual discrimination in rats with impaired retinal mitochondrial function. Other LLLT research studies utilized a variety of wavelengths (633�1064 nm), daily doses (1�60 J/cm2), fractionation sessions (1�6), and power densities (2�250 mW/cm2) which ultimately characterized effective LLLT parameters for both rats and humans. �
By way of instance, researchers evaluated in rats the effects of different LLLT doses in vivo on brain cytochrome oxidase activity, at either 10.9, 21.6, 32.9 J/cm2, or no LLLT. Treatments were utilized for 20, 40, and 60 min through four 660-nm LED arrays with a power density of 9 mW/cm2. One day after the LLLT session, the brains of the rats were extracted, frozen, sectioned, and processed for cytochrome oxidase histochemistry. A 10.9 J/cm2 dose increased cytochrome oxidase activity by 13.6 percent. A 21.6 J/cm2 dose developed a 10.3 percent increase. A non-significant cytochrome oxidase increase of 3 percent was found after the highest 32.9 J/cm2 dose. Responses of brain cytochrome oxidase to LLLT in vivo were characterized by hormesis, with a low dose being stimulatory while higher doses were less effective. �
The first demonstration that LLLT increased oxygen consumption in the rat prefrontal cortex in vivo was demonstrated by another research study. Oxygen concentration in the cortex of rats was measured utilizing fluorescence-quenching during LLLT at 9 mW/cm2 and 660 nm. LLLT promoted a dose-dependent increase in oxygen consumption of 5 percent after 1 J/cm2 and 16 percent after 5 J/cm2. Because oxygen is utilized to develop water within mitochondria in a response developed by cytochrome oxidase, more cytochrome oxidase activity should promote more oxygen consumption. �
LLLT can also offer several benefits over other types of stimulation because LLLT non-invasively targets cytochrome oxidase, a fundamental enzyme utilized for energy production, with promoted expression associated with energy increase. LLLT is mechanistically specific and non-invasive while transcranial magnetic stimulation may be non-specific, prolonged forehead electrical stimulation may increase muscle spasms and deep brain or vagus nerve stimulations are invasive. �
Transcranial Lasers on Cognitive and Emotional Functions
LLLT through commercial low-power sources, such as FDA-cleared laser diodes and LEDs, is a highly promising, affordable, non-pharmacological alternative treatment option for improving cognitive brain function. LLLT offers safe doses of light energy which regulate and maintain neuronal functions, however, these are low enough to not damage the brain. In 2002, the FDA approved LLLT for pain relief in cases of head and neck pain, arthritis and carpal tunnel syndrome. LLLT has been utilized non-invasively in humans after ischemic stroke to improve neurological functions. It also improved recovery and ultimately reduced fatigue after exercise. One LLLT stimulation session to the forehead, as demonstrated in another research study, developed a considerable antidepressant effect in patients with depression. No adverse side effects were found either immediately nor at 2 or 4 weeks after LLLT. Therefore, LLLT treatments have been demonstrated to be safe and effective in humans. Although LLLT has been determined to be safe and it received FDA approval to be utilized for pain treatment, transcranial lasers for the augmentation of cognitive brain function should be limited for further research studies until further outcome measures support this application for clinical utilization. �
Transcranial laser stimulation to the forehead was utilized in a placebo-controlled, randomized research study, to demonstrate the effects of cognitive tasks associated with the prefrontal cortex, including a psychomotor vigilance task, or PVT, and a delayed match-to-sample, or DMS, memory task. The PVT evaluates sustained attention, with patients remaining vigilant during delay intervals, and pushing a button when visual stimulation appeared on a monitor. The laser stimulation targeted prefrontal regions which are believed to be utilized in the sustained attentional processes of the PVT. The DMS task supports the prefrontal cortex as part of a network of frontal and parietal brain regions. �
Healthy patients received consistent wave near-infrared light intersecting cytochrome oxidase’s absorption spectrum, targetted to the forehead utilizing a 1064 nm low-power laser diode, also known as �cold laser�, which increases tissue penetration due to its long wavelength and has been utilized in humans for other health issues. The power density or irradiance, 250 mW/cm2, and the cumulative energy density or fluence, 60 J/cm2, were identical which demonstrated the benefits of psychological effects in another research study. This laser exposure develops negligible heat and no physical damage at the low power level utilized. This laser apparatus is utilized safely in a clinical setting by the supplier of the laser. Reaction time in the PVT was improved by the laser treatment, as demonstrated by a considerable pre-post reaction time effect associated with the placebo group. The DMS memory task also demonstrated considerable improvements in measures of memory retrieval latency and number of correct trials, when comparing the LLLT-treated with the placebo group as demonstrated in Figure 1. Self-reported positive and negative affective or emotional states were also measured utilizing the PANAS-X questionnaire before and 2 weeks after laser treatment. As compared to the placebo, treated patients demonstrated considerably improved affective states. We suggest that this type of transcranial laser stimulation may serve as a non-invasive and efficacious method and technique to augment cognitive brain functions associated with attention, memory, and emotional functions. �
Figure 1. Cognitive performance in the delayed match-to-sample (DMS) memory task was improved after transcranial infrared stimulation to the right forehead. The DMS task involves presentation of a visual stimulus (grid pattern) on a screen. Then the stimulus disappears, and the participant must remember the stimulus through a delay. Then two choices appear, and the participant must decide which of these two is identical to the previous stimulus (the �match�). Treated subjects showed faster memory retrieval (left panel) and increased number of correct trials (right panel) out of 30 trials when attempting to choose the correct grid pattern. The function of frontal cortex regions, implicated in the attentional mode network utilized during this visuospatial memory task, was augmented by the laser treatment. Compared to baseline, this treatment also increased by 5% the oxyhemoglobin concentration of the prefrontal cortex as measured by near-infrared spectroscopy, both during the laser stimulation and during post-treatment DMS performance (in preparation). The data for the treated group consisted of n = 10 males and n = 10 females; the control group also consisted of n = 10 males and n = 10 females. *Significant treatment by pre-post score interaction, p < 0.05.
LLLT’s bioenergetics mechanisms associated with cognitive augmentation may also be associated in its neuroprotective effects. LLLT’s stimulation of mitochondrial respiration should improve cellular function due to increased metabolic energy and cellular survival after injury due to the antioxidant effects of increases in cytochrome oxidase and superoxide dismutase. �
Laser transmittance of the 1064-nm wavelength at the forehead LLLT site was estimated in a post-mortem human specimen, which demonstrated that approximately 2 percent of the light passed through the frontal bone. This yielded an absorption coefficient of a = 0.24, similar to the demonstrated a = 0.22 transmittance through cranial bone for this wavelength. Furthermore, it was estimated that about 1.2 J/cm2 of the 60 J/cm2 LLLT dose applied reached the surface of the prefrontal cortex. This value is similar to 1 J/cm2, the peak effective LLLT dose in neuron cultures for increasing cytochrome oxidase activity. �
Transcranial absorption of photon energy by cytochrome oxidase, the terminal enzyme in mitochondrial respiration, is associated as the bioenergetic mechanism of action of LLLT in the brain. Transcranial LLLT up-regulates cortical cytochrome oxidase and improves oxidative phosphorylation. LLLT improves prefrontal cortex-related cognitive functions, such as sustained attention, extinction memory, working memory, and affective state. Transcranial infrared stimulation may be utilized effectively to support neuronal mitochondrial respiration as a new non-invasive, cognition-improving intervention in animals and humans. This fascinating new treatment approach should also be able to affect other brain functions associated with the neuroanatomical site stimulated and the stimulation parameters utilized. �
Low-level laser therapy, or LLLT, and other types of transcranial lasers are non-invasive, low-powered lasers which are now being utilized in specific cortical regions of the brain to improve physiological responses and cognitive function. Many research studies have demonstrated that transcranial lasers can ultimately improve attention, memory, and reactions, where many other research studies have also demonstrated that these can also help improve depression and possibly even Alzheimer’s disease. Although further research studies are still required, the outcome measures are promising. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
According to research studies, transcranial infrared laser stimulation, as well as other types of transcranial lasers, utilized on frontal cortex functions can improve sustained attention and working memory, among other brain functions. Transcranial laser stimulation regulates and maintains brain functions and may promote neurotherapeutic effects in a non-destructive and non-thermal manner. Researchers determined through the first controlled research study that transcranial laser stimulation improves human cognitive and emotional brain functions. 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
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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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