Prenatal and Postnatal Epigenetic Programming (PreP and PEP): Implications for GI, Immune and Neuronal Function in Autism

Oxidative stress and impaired methylation are implicated in causing autism, acting via their epigenetic influence over gene expression. However, fetal and postnatal development rely upon different nutritional resources, each presenting distinctive sources of risk. Dr. Deth will discuss the factors affecting PreP and PEP in the context of neurodevelopment, autoimmunity and gastrointestinal function, each of which contribute to autism spectrum disorders.

Richard C. Deth, PhD

Dr. Richard Deth is a professor of pharmacology at Northeastern University in Boston. He earned a B.S. in Pharmacy, 1970, from SUNY at Buffalo; and a Ph.D. in Pharmacology from University of Miami, 1975. Following their discovery of dopamine-stimulated phospholipid methylation in the late 1990’s, his lab focused on the folate and B12-dependent enzyme methionine synthase and its regulation by redox. His lab is investigating the fundamental role of redox signaling and methylation status, especially as it relates to autism, Alzheimer’s disease and other neurological disorders