Looking at Glutamate in Underlying Infections & Immune Dysfunction (PANS, PANDAS, AE, Lyme, etc)


Pediatric Acute-onset Neuropsychiatric Syndrome (PANS), Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS) diagnosis has jumped to 1 in 200 hundred and is becoming more and more common. These disorders are distinguishing by an often striking onset of neuropsychiatric symptoms in response to immune activation and possibly misdirected immune response. While PANS can be triggered by numerous infections, PANDAS is just associated with the strep infection.

Symptoms of PANS & PANDAS

What is Glutmate’s Role in Underlying Infections

Pediatric Acute-onset Neuropsychiatric Syndrome (PANS), Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS), Lyme, Chronic Inflammatory Response Syndrome (CIRS), etc are being diagnosed more and more frequently.  So what is the connection between these underlying infections and glutamate (click here, for What is Glutamate)? Microglia are a type of glial cell located in the brain and the spinal cord. They act as the first and main* form of immune defense in protection against foreign invaders in the central nervous system (CNS). When the microglia are chronically activated (either from single stimuli or multiple stimuli such as vaccines, physical injuries, or chronic underlying infections) they result in disruption of brain function and neuron loss due to their surge of inflammatory cytokines and excitotoxic levels of glutamate. Just to clarify, the immune response to the infection causes a surge of glutamate, which overexcites the brain and leads to imbalances in other neurotransmitters (GABA, serotonin, dopamine, etc.) and cellular death.

In fact, most viruses don’t directly damage the brain, they cause the brain to activate its glutamate receptors, its immune receptors, and cytokine receptors. This process is often referred to as a ‘glutamate storm and is actually what causes the damage, not the virus itself. If you block glutamate receptors in measles encephalitis, you have no damage. This is also a major mechanism of Lyme disease. It is not uncommon for some of these underlying infections to start to utilize glutamate as its energy source.  Borrelia and streptococcus are great examples of how pathogens can flourish in glutamate-rich environments. This creates a cyclical immune/inflammation/glutamate response, allowing for the infections to thrive.

Additionally, when you have excess glutamate in response to underlying infection, it contributes to additional symptoms like obsessive-compulsive disorder (OCD), anxiety, depression, sleep disturbances, seizures, tics all of which have been scientifically directly linked to be caused from excess glutamate.

So for those with chronic underlying infections, they become hypersensitive to glutamate.  Allowing for even low levels of glutamate to trigger a response.  Some are able to regulate back to ‘normal’ once a perceived invader is gone, however, some cells can take a long time not to be sensitive (chronically in stress response) once a stressor is gone.

Why Would REID Be Important When Struggling With Underlying Infections & Immune Activation?

Consuming an excess amount of free glutamate can disrupt proper glutamate signaling. Working to lower dietary exposure to free glutamate through REID (click here for what is REID) can not only help to regulate proper glutamate signaling, but it can also help to calm microglial activation. Keep in mind, over 70% of your immune system is in your gastrointestinal tract, which is lined with glutamate receptors. According to Dr. Russell Blaylock, when one consumes free glutamate/MSG, the MSG alone can reactivate microglia and trigger the cyclical inflammatory immune response and cell danger response. This may explain why many with underlying infections may not tolerate higher glutamate foods like, gluten, dairy, soy, corn and processed food. It is important to use diet to normalize this inflammatory signaling and keep intrinsic glutamate (glutamate produced by the body) levels low. Restoring proper nutrient levels can also help calm this glutamate storm and restore proper immune function.

Many REID families struggling with underlying infections, have to utilize options to help combat these underlying infections in addition to the diet. Some examples include herbal protocols, homeopathy, pharmaceuticals, intravenous immunoglobulin (IVIG), etc. You may want to refer to this list to help navigate additional ways to restore glutamate balance and how to use herbs to combat these underlying infections and calm microglial activation, https://nourishedblessings.com/lowering-glutamate-protecting-against-glutamate-damage/


While some of these diagnoses are clinically diagnosed, there are some tests you can run to get a better idea as to what underlying infections you may be struggling with.  Keep in mind, some could very well be struggling with something outside the scope of these tests.

Looking for more information on PANS/PANDAS? Take a look at the Pediatric Research and Advocacy Initiative

Some* of the Science

This is not a comprehensive list, simply some articles I have found along the way.

Over 70% of your immune system is in the gastrointestinal tract. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2515351/

“Other chronic viral infections interfere with the GAD enzyme and some microbes like streptococcus flourish in a glutamate rich environment, thus many children with pandas and autism carry an ongoing infection with strep.” (http://www.holistichelp.net/blog/how-to-increase-gaba-and-balance-glutamate/)

“When activated by proinflammatory stimuli, microglia release substantial levels of glutamate, and mounting evidence suggests this contributes to neuronal damage during neuroinflammation.” “These findings indicate that a considerable degree of the neurodegenerative consequences of neuroinflammation may result from conversion of oxidative stress to excitotoxic stress. This phenomenon entails a biochemical chain of events initiated by a programmed oxidative stress and resultant mass-action amino acid transport. Indeed, some of the neuroprotective effects of antioxidants may be due to interference with these events rather than direct protection against neuronal oxidation.” Glutamate release from activated microglia requires the oxidative burst and lipid peroxidation https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1949347/

“The interaction between immune receptors within the central nervous system (CNS) and excitatory glutamate receptors trigger a series of events, such as extensive reactive oxygen species/reactive nitrogen species generation, accumulation of lipid peroxidation products, and prostaglandin activation, which then leads to dendritic retraction, synaptic injury, damage to microtubules, and mitochondrial suppression” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157093/

“Studies have shown that proinflammatory cytokines can activate a release of excitotoxins from microglia and astrocytes and that excitotoxins can likewise activate the release of immune proinflammatory cytokines from these same cells.[,,,] It is important to appreciate that exposure to individual proinflammatory cytokines are not neurodestructive, but that in certain combinations, such as IL-1 and tumor necrosis factor-alpha (TNF-alpha), destructive reactions can be robust.[,] The evidence strongly suggest that it is the combination of proinflammatory cytokines and excitotoxins that lead to neurodegeneration, rather than inflammation alone. Subtoxic concentrations of glutamate, when combined with subtoxic concentrations of lipopolysaccharide (LPS) or proinflammatory cytokines, become fully neurotoxic.[] Because both proinflammatory cytokines and excitotoxin release occur simultaneously, one would expect to see a synergistic neurodestructive cascade set in motion [Figure 3]. A number of studies have confirmed this destructive interaction.[,] This synergism between the immune system and excitotoxic levels of glutamate, aspartate, and QUIN also have similar effects on the BBB, brain vasculature, development of edema, and metabolic changes seen with TBI.[,,,,,]” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157093/

“Both immune mediators and excitatory amino acids can be generated and secreted by activated microglia, astrocytes, and oligodendroglia. Although astrocytes are the main repository for glutamate and aspartate, activated microglia can release substantial amounts of these excitatory amino acids into the extraneuronal space.” “It has been shown that even very high levels of proinflammatory cytokines cannot damage neurons except in the presence of microglia.[] Excitotoxins, also released by activated microglia, appear to be the most toxic component released by the microglia.[,,,,,]” “In fact, compelling evidence suggests that proinflammatory cytokines may not kill neurons directly but do so by enhancing excitotoxicity” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157093/

“As stated, several studies have shown that repetitive injuries are more damaging than single concussion of the same severity, even when separated by several months.[,]” “It is also known that systemic immune activation can worsen existing brain pathology by a similar mechanism, that is, by stimulating already primed microglia.[,,] In a real world situation, these players would be exposed to recurrent infections, and other systemic immune activating events, that would add to existing brain immune activation. Stress, for example, has been shown to increase brain microglial priming and activation, as well as increased brain ROS/RNS and lipid peroxidation (LPO).[,https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157093/

“Systemic immune stimulation has been shown to activate microglia within the brain, yet even intense systemic immune stimulation does not lead to neurodegeneration, unless there exists preexisting brain pathology.[,] Alterations in brain function, such as fatigue, sleep disturbances, cognitive dysfunction, anxiety, and depression, associated with systemic immune stimulation, is known as sickness behavior. Studies have shown that delayed symptoms, especially depression and cognitive dysfunction, resemble human disorders previously not thought to be related to immune stimulation of the brain.[,] More recent studies have also linked these behaviors and cognitive impairments to excess excitatory amino acids in specific brain areas.[,,]” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157093/

“The presence of systemic immune activation from infections or any cause occurring throughout life has the potential to accelerate and enhance brain immunoexcitotoxicity. One must also consider other sources of systemic immune stimulation, including that from infectious illnesses, vaccinations, exposure to pesticides and industrial chemicals, and even stress. Stress has been shown to prime microglia and evoke microglial activation.[]” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157093/

“Compelling research has linked excess glutamate stimulation and/or elevations of proinflammatory cytokines to a number of neuropsychiatric and behavioral conditions, many of which are seen with CTE. These include panic attacks, aggressive behavior, suicide, obsessive-compulsive disorder, anxiety, and depression.[,,,,,]” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157093/

“The interaction between glutamate receptors and specific cytokine receptors has been shown to result in a hyperreactive response of the microglia that was primed by the initial traumatic head injury or other events. Priming can occur not only from the initial impact, but also from systemic infections, certain toxic environmental exposures, including mercury, pesticide/herbicides, and latent virus infections within the brain. The latter may include cytomegalovirus and herpes simplex viruses. Once primed, subsequent injuries can result in a hyperactive response of the microglia, resulting in a several fold higher release of immune cytokines, chemokines, and other immune mediators, as well as a massive release of the excitotoxins—glutamate, aspartate, and quniolinic acid. Crosstalk between proinflammatory cytokines and glutamate receptors accelerate and worsen neurodegeneration in the affected areas. The frontal lobes, hippocampus, and parietal lobes show the greatest sensitivity to trauma-induced immunoexcitotoxicity. Both inflammatory cytokines and excitotoxins can dramatically increase the generation of reactive oxygen and reactive nitrogen intermediates and an array of LPPs, both of which interfere with glutamate clearance, thus magnifying immunoexcitotoxicity over a prolonged period. Repeated trauma to the brain may prevent the normal microglial switching from a proinflammatory mode to a reparative mode, resulting in chronic microglial immunoexcitotoxic activity and subsequent neurodegeneration. And, as demonstrated, several studies have shown that high levels of glutamate and quniolinic acid can significantly increase the deposition of hyperphosphorylated tau protein resulting in the observed NFT accumulation.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157093/

“Some cytokines like IL-1β and TNF induce neurotoxicity through elevated glutamate production that results in neuronal excitotoxic death [16]. The inactivation of IL-1β and TNF using neutralizing antibodies significantly reduced neuronal death in SK-N-SH cells induced by West Nile Virus [17]. Neuroinflammation and both cytotoxic and vasogenic edema were reduced in IL-1 type 1 receptor-deficient mice conferring neuroprotection in stroke [18]. IL-1β also promotes oligodendrocyte death through glutamate excitotoxicity [19]” https://www.hindawi.com/journals/mi/2013/480739/

A common contributing cause of increased excitatory stimulation is elevated glutamate as a result of an overly active immune system. Glutamate is highly excitatory and is described as “excitotoxic” because elevated levels can damage neurons.  Elevated glutamate could be a root cause behind calming neurotransmitter (serotonin and GABA) imbalances and a consequence of imbalances in the immune system. Glutamate is highly influenced by the presence of both acute and chronic inflammatory responses.” https://neuroendoimmune.wordpress.com/2013/04/02/neuroimmune-transmitters-glutamate/

Elevated amounts of glutamate, which acts as a neurotransmitter but is also a neurotoxin, are a hallmark of the autoimmune neurological disease multiple sclerosis and may contribute to its pathology. The discovery that a receptor for glutamate can inhibit the development of autoimmunity and protect from neuroinflammation in a mouse model of multiple sclerosis suggests that glutamate may also have a protective role and that its receptor may represent a therapeutic target” Glutamate joins the ranks of immunomodulators https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2997749/

“A compelling amount of research has shown that repeated stimulation of the systemic immune system results in first priming the brain’s immune cells (called microglia) in the developing brain, followed by an intense microglial reaction with each successive series of vaccinations. When activated, especially chronically, microglia secrete a number of inflammatory cytokines, free radicals, lipid per oxidation products, and two excitotoxins—glutamate and quinolinic acid. Because of the critical dependence of the developing brain on a timed sequence of cytokine and excitatory amino acid fluctuation, sequential vaccination can result in alterations in this critical process that cause brain damage and abnormal pathway development. The evidence suggests that this overstimulation and persistent activation of the microglia is the central mechanism causing autism.” (http://beyondhealth.com/media/wysiwyg/kadro/articles/ExcessiveHungerandAutism.pdf)

“This mechanism involves activation of the brain’s innate immune system, primarily the microglia, with a release of neurotoxic concentrations of ex- citotoxins and pro-inflammatory cytokines, chemokines and immune mediators. A large number of studies suggest that excitotoxicity plays a significant role in the neurotoxic action of a number of metals, including aluminum. Recently, re- searchers have found that while most of the chronic neurodegenerative effects of these metals are secondary to prolonged inflammation, it is the enhancement of excitotoxicity by the immune mediators that is responsible for most of the metal’s toxicity. This enhancement occurs via a crosstalk between cytokine receptors and glutamate receptors.” http://www.geoengineeringwatch.org/documents/Aluminum-Blaylock.pdf

Anti-NMDA Receptor Encephalitis- The NMDA receptor (is one type of glutamate receptor highly concentrated in the brain) becomes attacked by antibodies as an immune response. Because of this, glutamate will start to build outside the NMDA receptor in the extracellular space and the nearby cells will start to signal additional glutamate in response to the stress (glutamate signaling is how the body signals stress/inflammation). With all of this extracellular glutamate, nearby cells/neurons adapt by adding additional glutamate receptors, which therefore make them more sensitive to glutamate (even to low levels-which becomes problematic with cell memory). These high levels of glutamate become excitotoxic, allowing for nearby cells to fire so rapidly that they die or cause severe mitochondrial dysfunction. This is a very similar reaction to what happens with a stroke which is often called a glutamate storm. High levels of glutamate also block the intake of cysteine into the cell through the glutamate/cysteine exchanger and this in tern reduces glutathione production, increases oxidative stress within cell, causes increased free radicals and this then leaks oxidative stress to extracellular region resulting in a vicious loop of damage to nearby cells. In other words, reducing glutamate signaling helps with cysteine uptake into cell and glutathione production. You will often hear that glutamate is actually what causes the damage, not the virus, and this is part of the reason why. This gets FAR FAR FAR more in depth but just wanted to put this here for now. http://www.ageofautism.com/2015/11/revisiting-anti-nmda-receptor-encephalitis-and-autism.html

“L-glutamate (L-Glu) is one of the most important excitatory neurotransmitters in the mammalian central nervous system (CNS). However, high concentrations of L-Glu cause excessive stimulation of L-Glu receptors and lead to neurotoxicity. Accordingly, the impairment of L-Glu transporters has been suggested to contribute to elevated extracellular L-Glu concentrations in inflammation; however, the specific role of such transporters remains unknown, as some inflammation models also cause cell death. In this study, we aimed to clarify the interaction between activated microglia and astrocyte L-Glu transporters in inflammation.Our findings suggest that activated microglia trigger the elevation of extracellular L-Glu through their own release of L-Glu, and astrocyte L-Glu transporters are downregulated as a result of the elevation of astrocytic intracellular L-Glu levels, causing a further increase of extracellular L-Glu. Our data suggest the new hypothesis that activated microglia collude with astrocytes to cause the elevation of extracellular L-Glu in the early stages of neuroinflammation.” https://www.ncbi.nlm.nih.gov/pubmed/23259598

“The vaccine is different from a natural infection in that the vaccine produces brain immune stimulation for very prolonged periods. It has been proven, in both animal studies and human studies, that systemic infections or immune activation by vaccines, rapidly activate the brain’s microglial system and can, in the case of vaccines, do so for prolonged periods. Once the primed microglia are reactivated by the subsequent vaccination or infection, the microglia activate fully and pour out their destructive elements as discussed above. With a natural infection, the immune system quickly clears the infection and then shuts off the immune activation, thus allowing repair of what damage was done. This shutting down of the microglia is very important. There is evidence that with repeated and excessive vaccine-triggered immune stimulation, the microglia do not shut down. So, we see that giving a live, immunosuppressant vaccine early in life can dramatically increase the risk of autoimmune disorders, increase microglial brain injury as well as increase the risk of infection by other immune-suppressing viruses and pathogenic organisms. Most of these will be spaced within one month of each other, which means the priming and activation cycle of the microglia will be continuous.” http://www.jpands.org/vol9no2/blaylock.pdf

“A newer study has shown conclusively, that mitochondrial activation using a vaccine adjuvant not only suppresses mitochondrial function but that the damage cause by this mitochondrial suppression is actually produced by excitotoxicity. Blocking excitotoxicity completely blocks the microglial-induced neurotoxicity and mitochondrial damage cause by the vaccine. A great number of studies have shown that activating the systemic immune system repetitively worsens neurological disorders caused by other things and can initiate neurodegeneration itself, that is prolonged. The inflammatory cytokines interact with glutamate receptors to dramatically increase excitotoxic damage. We know that autistic children have elevated CSF and blood levels of glutamate, which confirms the presence of the excitotoxic process.” http://www.ageofautism.com/2008/04/dr-blaylock-on.html

“As increasing evidence indicates that astrocytes and microglial cells play a major role in synapse maturation and function, and there is evidence of deficits in glial cell functions in ASDs, one current hypothesis is that glial dysfunctions directly contribute to their pathophysiology.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751265/

“Males also have a higher concentration of microglia earlier in life compared to females. This will make them more vulnerable to vaccines and immune activation. Microglia signal additional glutamate, allowing for increased sensitivity to glutamate. ” Males have overall more microglia early in postnatal development (postnatal day (P) 4), whereas females have more microglia with an activated/amoeboid morphology later in development, as juveniles and adults (P30-60). Finally, gene expression of a large number of cytokines, chemokines and their receptors shifts dramatically over development, and is highly dependent upon sex. ” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296888/

“Evidence indicates that children with autism spectrum disorder (ASD) suffer from an ongoing neuroinflammatory process in different regions of the brain involving microglial activation.” “It is plausible that by reducing brain inflammation and microglial activation, the neurodestructive effects of chronic inflammation could be reduced and allow for improved developmental outcomes. Future studies that examine treatments that may reduce microglial activation and neuroinflammation, and ultimately help to mitigate symptoms in ASD, are warranted.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523548/

“Two basic processes seem to be responsible for the chronic stimulation of brain immunity: repeated, closely spaced inoculation without allowing brain recovery, and inoculation with live viruses or contaminant organisms that persist in the brain.” http://www.jpands.org/vol9no2/blaylock.pdf

“A compelling amount of research has shown that repeated stimulation of the systemic immune system results in first priming the brain’s immune cells (called microglia) in the developing brain, followed by an intense microglial reaction with each successive series of vaccinations. When activated, especially chronically, microglia secrete a number of inflammatory cytokines, free radicals, lipid per oxidation products, and two excitotoxins—glutamate and quinolinic acid. Because of the critical dependence of the developing brain on a timed sequence of cytokine and excitatory amino acid fluctuation, sequential vaccination can result in alterations in this critical process that cause brain damage and abnormal pathway development. The evidence suggests that this overstimulation and persistent activation of the microglia is the central mechanism causing autism.” (http://beyondhealth.com/media/wysiwyg/kadro/articles/ExcessiveHungerandAutism.pdf)

“Growing evidence indicates that there is a close correlation between brain inflammation (by microglial released inflammatory cytokines and glutamate) and seizures, just as we see with excessive brain immune stimulation with vaccines. Using lipopolysacchride as a vaccine-based immune stimulant, scientists have induced seizures in experimental animals of various species.57,58 A considerable amount of evidence links excitotoxicity and seizures. In addition, a number of the newer anti-seizure medications work by blocking glutamate receptors or preventing glutamate release. One of the central mechanisms linking excessive immune stimulation with seizures, as with vaccines, is the induced release of the excitotoxin glutamate and quinolinic acid from immune stimulated microglia and astrocytes.59-61 In many cases these seizures are clinically silent or manifest as behavioral problems, often not recognized by pediatricians as seizures. Yet, they can alter brain function and eventually result in abnormal brain development. Even the CDC and American Academy of Pediatrics recognize that infants and children with a history of seizure should not be vaccinated. It is also known that autistic children who regress, that is begin to show a sudden worsening of mental development, have a significantly higher incidence of seizures, both clinical and subclinical, than those who do not regress. Interestingly, studies have shown that during early brain development after birth the number of glutamate receptors (that trigger the seizures) increase steadily until the age of two when it peaks.62 Thereafter they decline in number. This means that the immature brain is significantly more susceptible to seizures than the more mature brain and this is when your child is being given 24 vaccine inoculations, many of which are associated with a high incidence of seizure.” Growing evidence indicates that there is a close correlation between brain inflammation (by microglial released inflammatory cytokines and glutamate) and seizures, just as we see with excessive brain immune stimulation with vaccines. Using lipopolysacchride as a vaccine-based immune stimulant, scientists have induced seizures in experimental animals of various species.57,58” http://articles.mercola.com/sites/articles/archive/2008/03/14/the-danger-of-excessive-vaccination-during-brain-development.aspx

“The autism spectrum disorders (ASD) are a group of related neurodevelopmental disorders that have been increasing in incidence since the 1980s. Despite a considerable amount of data being collected from cases, a central mechanism has not been offered. A careful review of ASD cases discloses a number of events that adhere to an immunoexcitotoxic mechanism. This mechanism explains the link between excessive vaccination, use of aluminum and ethylmercury as vaccine adjuvants, food allergies, gut dysbiosis, and abnormal formation of the developing brain. It has now been shown that chronic microglial activation is present in autistic brains from age 5 years to age 44 years. A considerable amount of evidence, both experimental and clinical, indicates that repeated microglial activation can initiate priming of the microglia and that subsequent stimulation can produce an exaggerated microglial response that can be prolonged. It is also known that one phenotypic form of microglia activation can result in an outpouring of neurotoxic levels of the excitotoxins, glutamate and quinolinic acid. Studies have shown that careful control of brain glutamate levels is essential to brain pathway development and that excesses can result in arrest of neural migration, as well as dendritic and synaptic loss. It has also been shown that certain cytokines, such as TNF-alpha, can, via its receptor, interact with glutamate receptors to enhance the neurotoxic reaction. To describe this interaction I have coined the term immunoexcitotoxicity, which is described in this article.” A possible central mechanism in autism spectrum disorders, part 1. https://www.ncbi.nlm.nih.gov/pubmed/19043938

“Multiple lines of evidence suggest that inflammation and glutamate dysfunction contribute to the pathophysiology of depression. Peripheral inflammation leads to microglial activation which could interfere with excitatory amino acid metabolism leading to inappropriate glutamate receptor activation” https://www.ncbi.nlm.nih.gov/pubmed/18567974

“Auism spectrum disorder (ASD) now affects one in 68 births in the United States and is the fastest growing neurodevelopmental disability worldwide. Alarmingly, for the majority of cases, the causes of ASD are largely unknown, but it is becoming increasingly accepted that ASD is no longer defined simply as a behavioral disorder, but rather as a highly complex and heterogeneous biological disorder. Although research has focused on the identification of genetic abnormalities, emerging studies increasingly suggest that immune dysfunction is a viable risk factor contributing to the neurodevelopmental deficits observed in ASD. This review summarizes the investigations implicating autoimmunity and autoantibodies in ASD.” https://www.ncbi.nlm.nih.gov/m/pubmed/28340985/

“Inflammatory cytokines interfere with the regulation of the neurotransmitter, glutamate. Glutamate is an excitatory neurotransmitter that, if left to go wild, can pound our NMDA receptors in the brain and wreak major havoc. No one wants overexcited NMDA receptors, and clinical depression is one among many nasty brain issues that can be caused by overexcitement. Astrocytes, little clean-up cells in the brain, are supposed to mop up excess glutamate to keep it from going nutso on the NMDA. Turns out inflammatory cytokines interfere with the clean-up process. The horse tranquilizer (and club drug) ketamine, when administered IV, can eliminate symptoms of severe depression pretty much immediately in some cases (do NOT try this at home) (2). Ketamine helps the astrocytes mop up glutamate, and it is assumed that this is how ketamine instantly cures depression. Unfortunately, the effects of ketamine don’t last, otherwise it would be a nifty tool, indeed.” https://www.psychologytoday.com/blog/evolutionary-psychiatry/201103/depression-caused-inflammation-thus-other-diseases-civilization

Immune Abnormalities in Autism Spectrum Disorder—Could They Hold Promise for Causative Treatment?
“There is evidence of altered immune function both in cerebrospinal fluid and peripheral blood. Several studies hypothesize a role for neuroinflammation in ASD and are supported by brain tissue and cerebrospinal fluid analysis, as well as evidence of microglial activation. It has been shown that immune abnormalities occur in a substantial number of individuals with ASD”
What else is a byproduct of microglial activation? Glutamate https://link.springer.com/article/10.1007/s12035-017-0822-x

Cytokines and Chemokines at the Crossroads of Neuroinflammation, Neurodegeneration, and Neuropathic Pain https://www.hindawi.com/journals/mi/2013/480739/

Dr. Russell Blaylock has a ton of information on the role of immune activation and the damages caused by the cytokine storm and excess glutamate. Some of his videos can be found below.

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