In June, Dr. Russell Blaylock published a paper which describes aluminium’s neurotoxic properties and the connection between childhood vaccines which contain aluminium and autism spectrum disorder (“ASD”).
“In this paper, I offer a well-demonstrated mechanism that would explain why a subset of children develop autism after vaccines,” he wrote.
He notes that it is not only vaccination after birth that triggers ASD, but that a pregnant mother receiving a vaccine could also trigger the process. Referring to previous research, he said, “The possibility of immune priming of the infant by vaccinating the woman during pregnancy was entertained. This would represent the 1st priming event.” And then, “after birth, subsequent vaccinations would further prime the child” for developing ASD.
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We are republishing Dr. Blaylock’s June paper in a series of articles. Although it is not overly technical, it does include some terms and concepts we may not be familiar with. By publishing it piecemeal, we are hoping our readers do not become overwhelmed by jargon that might be the case had they been faced with the entire paper at once. Also, it might give an opportunity for pause, to look up and familiarise themselves with terms as required.
You can read Part 1 HERE, where Dr. Blaylock provides an overview of the factors that contribute to a person developing an autism spectrum disorder. You can read Part 2 HERE, where he describes the effects that excessive stimulation of the immune system triggers damage, and even kills, nerve cells. If you would like to read the paper in one sitting, you can do so HERE. Please note, we have not included the references noted in the paper as originally published. And we have made some minor edits to convert American English to British English and preferred stylisation, e.g. removal of Oxford commas.
Autism Spectrum Disorders: Is Immunoexcitotoxicity the Link to the Vaccine Adjuvants? The Evidence
By Russell L. Blaylock, as published by Science, Public Health Policy and the Law on 1 June 2025
“I coined the term ‘immunoexcitotoxicity,’ which describes the interplay between immune activation and excitotoxic neuronal injury.”—Russell L. Blaylock, Autism Spectrum Disorders: Is Immunoexcitotoxicity the Link to the Vaccine Adjuvants? The Evidence
[Note from The Exposé: Microglia are the primary immune cells of the central nervous system (“CNS”), acting as the first and main form of active immune defence in the brain and spinal cord. They account for approximately 5–10% of all cells in the brain. Glutamate is the most abundant excitatory neurotransmitter in the nervous system, playing a crucial role in learning, memory and overall brain function. Microglia play a critical role in regulating glutamate homeostasis, the maintenance of a stable internal environment despite changes in external conditions. The release of glutamate by activated microglia contributes to excitotoxicity, a key mechanism of neurodegeneration.]
Table of Contents
- Microglial Activation and Priming
- Baseline Microglial Function in Normal Development
- Microglia and Neuronal Migration in Different Areas of the Brain
- Why are Males Affected More Often?
- Vaccine-Induced Microglial Priming
- Consequences of Repeated Immune Stimulation
- Disrupted Pruning and Learning
- Cerebellar Development in Autism Spectrum Disorders: Microglial Activation in the Cerebellum in Autism Spectrum Disorders Neurodevelopment and the Microglia
Microglial Activation and Priming
Baseline Microglial Function in Normal Development
Brain Development and Cytokines and Excitotoxins
Stress accelerates the colonisation of microglia in the postnatal brain. In addition, the timing of the switch from a resting (ramified) to an activated (ameboid) state profoundly affects neurodevelopment. As we shall see, this is important because variations in microglial activation contribute to neurodevelopmental differences between males and females.
Microglia are known to be involved in all aspects of neurodevelopment, including synaptogenesis, neuron elimination (pruning), angiogenesis, migration, proliferation, differentiation, migration of progenitor cells, and synaptic refinement. The release of chemokines, cytokines and excitotoxins from these cells plays a vital role in the ultimate architectonic development of the brain, its physiology and biochemistry. Glutamate uptake proteins are negatively affected by inflammatory cytokines and free radicals. Tumour necrosis factor-alpha and IL-1ß are the most involved proinflammatory cytokines in impaired glutamate transport. Free radicals also impair these transport proteins.
Microglia are not derived from macrophages/monocytes during development but are produced within the brain, except for the cerebellum and retina. From embryonic day 12 onward, increasing numbers of microglia are found throughout the developing cortex. The densest population of microglia is seen in the two most proliferative zones of the developing brain: the ventricular zone (“VZ”) and the subventricular zone (“SVZ”). Activation of microglia in these zones, as occurs with mass vaccination administered closely together, would be expected to affect neuron development in these areas negatively.
During early brain development, a specialised glial scaffolding network, derived from astrocytic cells, is formed, known as the radial glial cell network. The progenitor cells for both the glia and neurons migrate along this radial glial network to form the multilayer cortical cell layer. Microglia, with their pulsed release of glutamate, play a major role in this process. These microglia are derived from mesodermal cells (macrophage population) progenitors at approximately 4.5 weeks of gestation in the human brain, during the development of blood circulation. These macrophage progenitors enter via the meninges and choroid plexus, then travel to the germinal zones to form the functional zones of the brain. Factors controlling this process include cytokines, chemokines, as well as morphogens, growth factors and glutamate released from microglia. The microglia use axons, perivascular sheaths and radial glia cells as a migratory scaffold. It is during this period of migration that the six-layered cortex eventually forms. In autism, this period of migration and cortical formation is often disrupted by alterations in microglial function, leading to atypical cortical development and neurodevelopmental abnormalities.
Disruption of the column architecture and connectivity of the columns appears to be characteristic of autism spectrum disorders. Damarla demonstrated this disconnection by examining high-functioning autistics using a combination of behavioural testing, functional MRIs and measures of functional connectivity between the higher-order working memory executive area and visuospatial regions, as well as between frontal and parietal-occipital regions. Others demonstrated functional connectivity defects between the anterior and posterior insula, as well as between these regions and brain areas involved in emotional and sensory processing.
Using DTI imaging (Diffusion Tensor Imaging), researchers described significant abnormalities in the white matter development of the cingulum bundle among 21 adolescents with ASD compared to healthy controls. They also found that measures of tract malformation within the cingulum bundle had a worse prognosis.
A recent study found that synaptogenesis and synaptic pruning follow a programmed timeline specific for each area of the developing brain. Synaptic pruning begins to decline at puberty and is complete within the prefrontal cortex during adolescence. Elimination of synapses in the CNS continues well into the third decade.
During neurodevelopment, glutamate receptors, as well as microglia and astrocytes, play a special role in every aspect of brain development. Astrocytes are the primary depository of glutamate, and microglia contain a significant amount of glutamate, which is released in response to inflammatory stimulation. As the NMDA [N-methyl-D-aspartate] receptors control intracellular calcium and are located on the growth cones used to guide neural connections, these receptors are implicated in regulating neural migration, which is crucial for proper neurodevelopment.
NMDA receptors generate calcium waves that control the migration of these connections and neurons. Secreted glutamate controls calcium waves. Glutamate gradients, ultimately responsible for these neuronal and axonal migrations, are being altered by systemic vaccination during the childhood vaccination process via immunoexcitotoxicity. Variations in the oscillation of calcium waves by NMDA receptors on the growth cones will alter this migration. High levels of glutamate can increase migration, and low levels reduce it by controlling these calcium waves. As with vaccination, immune stimulation can activate CNS microglia and astrocytes, which alters glutamate levels in the CNS.
Microglia and Neuronal Migration in Different Areas of the Brain
Microglia colonise the developing brain at significantly different rates. For example, in rats, and most likely humans, the first areas to be populated include the hippocampus, the amygdala and the cortex. Immune stimulation switching of the microglia also significantly affects brain maturation and development.
In the adult brain, the microglia are heterogeneously distributed, with the highest concentrations in the substantia nigra and second, in the hippocampus. In addition, microglia can migrate to areas of inflammation or invasion, as well as during development. These microglial cells are located throughout the entire central nervous system.
It should be appreciated that in addition to cytokines, growth factors and glutamate, microglia also release other excitotoxins, such as QUIN [quinolinic acid]. Under normal conditions, the kynurenine pathway releases mostly neuroprotective compounds, but in the face of inflammation, it switches to the production of the excitotoxin QUIN, which stimulates the NMDA glutamate receptor. So, we see a number of excitotoxins, such as glutamate, aspartic acid and QUIN, being released from activated microglia in the CNS under conditions of immune stimulation. Childhood vaccines could be such a stimulus even at the periphery of the body.
The activation of NMDA receptors on the growth cones is not only responsible for neuron and axon movement but also determines neurite outgrowth, motility, axon turning and Rho GTPases, which are all responsible for the brain’s eventual architecture. Therefore, we can see that the level and timing of glutamate pulses, as well as other immune excitotoxic factors, play a crucial role in brain development. The calcium gradients produced by the glutamate also play a major role in neuron proliferation, dendrite formation and extension, and growth cone function.
Within the intermediate germinal zone, a site of precursor cell proliferation, and the cortical plate, where neuronal differentiation occurs, further changes in brain maturation become apparent. The neurons express fully functional receptors. There is evidence that NMDA receptors appear in neurons of the cortical plate soon after they migrate from the ventricular zone (“VZ”) with fully functional receptors.
Why are Males Affected More Often?
Synaptic pruning is critical as neurodevelopment progresses because more synaptic connections are generated during development than are needed in the final cerebral and cerebellar architecture. This process is influenced by microglial activity, which varies between males and females. Males have a significantly greater number of microglia early after birth (P4-postnatal day 4) than females in regions of the brain concerned with cognition, learning and memory (hippocampus, amygdala and parietal lobe). It has also been shown that with a rise in testosterone in males, a dramatic increase in microglia in their brain occurs around E18 (embryonic day 18). This is a possible mechanism that could contribute to the early onset of neurological disorders such as dyslexia, ASD and ADHD in males.
Ironically, females have been shown to have more microglia than biological males, but this occurs much later during development, specifically between postnatal days 30 and 60. It was also demonstrated that most microglia in males at day P4 exhibited an activated morphology. In contrast, even at P30-P60, the females were more likely to have ramified (resting) microglia. The secretion of chemokines and cytokines has also been shown to be sex-related. This indicates drastic differences in susceptibility to induced ASD among biological males and females, based on the timing and activation of microglia in males and females.
Another enigma is the link between ASD and mitochondrial dysfunction. It is known that many children have borderline mitochondrial function and that, in one instance, a young girl developed autism after getting the childhood vaccine series. She was known to have a mitochondrial defect. It has been shown that even normal levels of glutamate can become excitotoxic when energy levels are deficient.
Mitochondrial disorders are known to be more common in males, making them more susceptible to immunoexcitotoxicity, especially at a young age.
Vaccine-Induced Microglial Priming
As with other immune cells, such as macrophages, microglia normally exist in a resting state. Once stimulated, enzymes responsible for producing pro-inflammatory cytokines are up-regulated, but the actual proteins are not released. If the immune system is activated subsequently, even several weeks to a month later, these primed microglia will release proinflammatory products at a rate about three times higher than normal. Once the primed microglia and astrocytes, including intracranial macrophages and mast cells, are activated and begin to release high levels of excitotoxins and proinflammatory cytokines, alterations in neurodevelopment and neurophysiology become apparent. One of the common observations made by observant parents is that often the child destined to develop ASD following vaccination is either systemically ill or has a localised infection, most often an ear infection, at the time the series of injections begins. The infection represents the first episode of immune stimulation (Figure 5). The microglial activation will do more than release proinflammatory cytokines and chemokines. They will also release high levels of excitotoxins, especially glutamate and QUIN (Figure 5).
As we shall see, this priming effect within the CNS will have a detrimental effect on neurodevelopment. The cytokines are elevated, as are the levels of released glutamate and other excitotoxic molecules, such as aspartate and QUIN. In an article by Wilcox and Jones, the question of the effects of vaccinating a pregnant woman is discussed. It has been shown that a mother can have an infection without a foetal infection, which can alter the child’s immune system, initiating priming. In addition to this, extensive research by Ashwood and Van de Water on maternal immune activation during pregnancy has demonstrated that alterations in the immune system during pregnancy can significantly impact the foetus, potentially leading to neurodevelopmental disorders, including autism. Their work highlights the critical role of maternal immune responses in influencing offspring’s brain development, further supporting the notion that immune activation in utero may contribute to developmental abnormalities. It could also elevate glutamate levels and trigger immunoexcitotoxicity, resulting in subsequent abnormal foetal development. The possibility of immune priming of the infant by vaccinating the woman during pregnancy was entertained. This would represent the 1st priming event.
Consequences of Repeated Immune Stimulation
After birth, subsequent vaccinations would further prime the child’s microglia and macrophages. As we shall see, this holds the potential to alter post-birth neurodevelopment significantly. One must also consider the sick child or the child with a preexisting active infection being vaccinated. Several paediatricians told me, as well as a number of mothers, that after the child developed autism, the parents were told by the doctor or the doctor’s nurse that “we frequently vaccinate such infected children.” It is often overlooked and unknown to paediatricians that the infection serves as a priming event, activating brain microglia and macrophages, and that this can significantly alter brain development during the critical period of neurodevelopment.
The nurse then injects the child with a series of injections, such as DTaP, MMR, or now the covid-19 injections. Often, the child will receive 7 to 9 injections on a single office visit. That represents a very large dose of immune adjuvants. Overall, these infants and children will receive more than 65 injections. We must acknowledge that this represents a substantial immune load and a very high dose of aluminium.
Some researchers appreciate the negative effects of pathogenic priming but attribute the link to ASDs to autoimmunity. I am convinced that the evidence indicates that the major damage of autoimmunity is excitotoxic. This is not to say that immune cytokines and chemokines do not affect neurodevelopment and neural physiology, because the evidence also suggests they play a significant, albeit not major, role.
One of the key events in the process of immunoexcitotoxicity is the physiological process of priming. When the immune system is stimulated to a moderate extent, the released proinflammatory cytokines stimulate the microglia, leading to an upregulation of enzymes that augment the immune and excitotoxic reactions. Yet, the immune products and excitotoxins are not released at that moment.
Subsequent injections, especially when spaced closely together, activate the brain’s microglia and astrocytes. When fully activated, they release high levels of pro-inflammatory cytokines and excitotoxins, including glutamate, aspartate and QUIN. At this stage, immunoexcitotoxicity occurs, significantly interfering with neurodevelopment through direct effects on both brain development and neurodegeneration.
Disrupted Pruning and Learning
Dendritic development begins early, with cortical neurons developing dendrites during the first two trimesters of gestation. The earliest formation of dendrites begins in the subplate and deeper cortical layers and accelerates from the third trimester, remaining high until the first postnatal year. This gives a broad period of vulnerability during which vaccination may interfere with brain development. In the human neocortex, dendritic development and moulding are most active during infancy and early childhood. This is when the childhood vaccine schedule begins and continues.
Cerebellar Development in Autism Spectrum Disorders: Microglial Activation in the Cerebellum in Autism Spectrum Disorders Neurodevelopment and the Microglia
Vargus and co-workers found that the cerebellum is the most heavily affected part of the brain among people diagnosed with autism, found at autopsy. In fact, there was an almost complete absence of Purkinje cells in the cerebellum. Interestingly, the cerebellum has many non-motor functions, including memory, language, emotional elaboration, reward and other higher brain functions.
Once the primed microglia and astrocytes, including intracranial macrophages and mast cells, are activated and begin to release high levels of excitotoxins and pro-inflammatory cytokines, alterations in neurodevelopment and neurophysiology become apparent. It has been shown within the cerebellum that GluA2 receptors, an AMPAR subunit that reduces Ca2+ influx, which is required for normal development of Purkinje cell dendrites, were defective. It was also shown that excess Ca2+ inhibited dendrite formation and maturation, which would occur with either GluA2‐lacking AMPAR insertion and/or overactivity of NMDARs. Increased trafficking of GluA2‐lacking AMPARs (Ca2+ permeable) occurs with inflammation, which is common in the brain in autism (Figure 3).
This effect of altered immunoexcitotoxicity and microglial/astrocyte activation was observed across different age groups of ASD patients, including both younger individuals and those up to 40 years old. Notably, microglial activation – initiating immunoexcitotoxicity – was evident early in development and persisted into adulthood. In the cerebrum, microglia play a crucial role in various aspects of brain development, which also extends to the cerebellum. Similarly, calcium oscillation induced by glutamate pulsation is fundamental to cerebellar development, just as in the cerebrum. Vargas et al. further noted that the greatest loss of neurons in autism occurs in the cerebellum, with the Purkinje cells being almost entirely absent. During cerebellar development, microglia undergo activation, which, when excessive, can lead to increased glutamate levels in the extracellular space. This excess glutamate may disrupt dendrite formation, contributing to long-term neurodevelopmental dysfunction, which may be influenced by repeated immune activation from multiple childhood vaccinations, with effects that persist into adulthood. In addition to the effects on neurodegeneration and neurodevelopment, we would also expect alterations in brain neurophysiology and biochemistry.
This consideration leaves open the possibility of multiple overlapping pathways contributing to ASD, reinforcing the connection between mass vaccination and ASD based on both clinical observations and research findings. Now that we have a mechanism that links exposure to multiple vaccines, spaced relatively close together, we have the necessary mechanism explaining the findings. This mechanism, immunoexcitotoxicity, logically links these findings to the vaccines.
The above is republished under Creative Commons Licence, CC BY 4.0 DEED Attribution 4.0 International.
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