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.”
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.”
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.”
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).”
Excerpt: “Because this neuroinflammatory process appears to be associated with an ongoing and chronic mechanism of CNS dysfunction, potential therapeutic interventions should focus on the control of its detrimental effects and thereby eventually modify the clinical course of autism.”
Exceprt:
” These results suggest that the IHg may be responsible for the increase in reactive glia.”
Excerpt:
“GFA in autism and autistic-like conditions was at a level almost three times that in the normal group. The results could implicate gliosis and unspecific brain damage in autism.”
