Glial Cells

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

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

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

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

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