Neurons operate under unique redox conditions, increasing their vulnerability to oxidative stress, and recent studies provide evidence of oxidative stress and neuroinflammation in autism. Impaired methylation is a consequence of oxidative stress, mediated in major part by inhibition of the folate- and colbalamin-dependent enzyme methionine synthase. Since methionine synthase activity is essential for dopamine-stimulated phospholipid methylation, some symptoms of autism may reflect impairment of this process. For example, dopamine D4 receptor activation plays an important role in gamma frequency synchronization of neural networks during attention, and autistic children display deficits in synchronization. This chapter reviews the metabolic events contributing to impaired methylation and examines the mechanisms by which they may contribute to neurodevelopmental disorders such as autism.
|Title of host publication||The Neurochemical Basis of Autism|
|Subtitle of host publication||From Molecules to Minicolumns|
|Number of pages||15|
|Publication status||Published - 2010|
ASJC Scopus subject areas