Glial Cells

Adjuvant / Aluminum / Autoimmunity / Blood brain barrier / Glial Cells / Immune / Toxicants

Slow CCL2-dependent translocation of biopersistent particles from muscle to brain

Excerpts:
“Intramuscular injection of alum-containing vaccine was associated with the appearance of aluminum deposits in distant organs, such as spleen and brain where they were still detected one year after injection.”

“Cerebral translocation was not observed after direct intravenous injection, but significantly increased in mice with chronically altered blood-brain-barrier.”

Conclusion
Nanomaterials can be transported by monocyte-lineage cells to DLNs, blood and spleen, and, similarly to HIV, may use CCL2-dependent mechanisms to penetrate the brain. This occurs at a very low rate in normal conditions explaining good overall tolerance of alum despite its strong neurotoxic potential. However, continuously escalating doses of this poorly biodegradable adjuvant in the population may become insidiously unsafe, especially in the case of overimmunization or immature/altered blood brain barrier or high constitutive CCL-2 production.

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  • April 4, 2013
20 Papers / ASD Subtypes / Autism Biomarkers / Autoimmunity / Genes / GI / Glial Cells / Immune / Neuroinflammation / Post-mortem / Review

Neuroinflammation and autism: toward mechanisms and treatments

Excerpts:

“In our clinical work and review of the literature, we have been impressed by the possible role of autoimmune disorders as influencing the pathophysiology of a distinct, objectively defined etiologic subtype of ASDs.”

“The notion that environmental factors contribute to ASD prevalence continues to evolve. Once-influential theories suggesting links among exposure to vaccines containing attenuated virus or toxins, conditions such as inflammatory bowel disease, and ASDs have fallen from favor since the retraction of a key study (Wakefield et al, 1998). It is important to emphasize, however, that the major reason for retraction was poor scientific method rather than theoretical flaws. Although ASDs are currently within the realm of psychiatrists and neurologists, it is becoming clear that at least some subtypes represent whole-body disorders, offering exciting new possibilities for therapy.”

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  • November 13, 2012
Astrocytes / Cytokines / Glial Cells / Immune / Inflammation / Neuroinflammation / Neurons / NF-KappaB / Post-mortem

Aberrant NF-KappaB Expression in Autism Spectrum Condition: A Mechanism for Neuroinflammation

Excerpt:
“In summary, NF-κB is aberrantly expressed in orbitofrontal cortex in patients with ASC, as part of a putative molecular cascade leading to inflammation, especially of resident immune cells in brain regions associated with the behavioral and clinical symptoms of ASC.”

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  • May 13, 2011
Glial Cells / Immune / Males

Microglial activation and increased microglial density observed in the dorsolateral prefrontal cortex in autism

Excerpt:
“CONCLUSIONS: The activation profile described represents a neuropathological alteration in a sizeable fraction of cases with autism. Given its early presence, microglial activation may play a central role in the pathogenesis of autism in a substantial proportion of patients. Alternatively, activation may represent a response of the innate neuroimmune system to synaptic, neuronal, or neuronal network disturbances, or reflect genetic and/or environmental abnormalities impacting multiple cellular populations.”

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  • August 15, 2010
Autoimmunity / Excitotoxicity / Glial Cells / Immune / Inflammation / Mitochondria / Neuroinflammation / Neurons / Oxidative Stress / Review / ROS / Toxicants

Bridging from Cells to Cognition in Autism Pathophysiology: Biological Pathways to Defective Brain Function and Plasticity

Excerpt:
“In autism, over-zealous neuroinflammatory responses could not only influence neural developmental processes, but may more significantly impair neural signaling involved in cognition in an ongoing fashion.”

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  • February 21, 2008
20 Papers / Antioxidant / Dendritic cells / Glial Cells / Glutamate / Lipids / Oxidative Stress / Purkinje cells / Regression / Review / ROS

The Neurobiology of Autism

Exceprts:
We also discuss evidence implicating oxidative stress, neuroglial activation and neuroimmunity in autism.

“Oxidative stress is another possible cause of Purkinje cell loss and other neuroanatomical changes described in autistic brains (reviewed in (37, 113)). Oxidative stress occurs when the levels of reactive oxygen species exceed the antioxidant capacities of a cell, often leading to cell death. Because of its very high oxygen demands and limited anti-oxidant capacity, the brain is thought to be relatively vulnerable to oxidative stress (111). Several studies have shown decreased levels of antioxidants such as superoxide dismutase, transferrin and ceruloplasmin in the blood or serum of patients with ASD (38, 108, 222). Significant elevations in biomarker profiles indicating increased oxidative stress, such as increased lipid peroxidation, have also been documented in autism (38, 107, 229).Interestingly, in one report the alterations in antioxidant proteins were linked specifically to regressive autism, suggesting a postnatal environmental effect (38). Polymorphisms in metabolic pathway genes may contribute to the increased oxidative stress in autism (108). Advanced glycationend products have also been reported to be elevated in both the brain tissue and serum of autistic patients, a change which can also lead to increased oxidative damage (23,110).”

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  • October 17, 2007

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