Ved Chauhan

TL;DR: ASD patients displayed an increased innate and adaptive immune response through the Th1 pathway, suggesting that localized brain inflammation and autoimmune disorder may be involved in the pathogenesis of ASD.

TL;DR: The diversity of opinions regarding the involvement of this important site in the pathology of autism will be observed, and points of consensus include presence of abnormal cerebellar anatomy, abnormal neurotransmitter systems, oxidative stress, Cerebellar motor and cognitive deficits, and neuroinflammation in subjects with autism.

TL;DR: Increases in oxidative stress with membrane lipid abnormalities, inflammation, aberrant immune response, impaired energy metabolism and excitotoxicity, leading to clinical symptoms and pathogenesis of autism is proposed.

TL;DR: Deterioration in the patterns of focal qualitative developmental defects in the brains of autistic subjects reflects multiregional dysregulation of neurogenesis, neuronal migration and maturation in autism, which may contribute to the heterogeneity of the clinical phenotype.

TL;DR: Results indicate altered regulation of transferrin and ceruloplasmin in autistic children who lose acquired language skills and it is suggested that such changes may lead to abnormal iron and copper metabolism in autism and that increased oxidative stress may have pathological role in autism.