CME Program: Metabolic Roles of Redox Regulation and Methylation: Part II: Autism-specific Aspects

There is extensive evidence indicating the occurrence of oxidative stress, neuroinflammation and impaired methylation in autism and related neurodevelopmental disorders. This knowledge has assisted in identifying treatment approaches which can provide therapeutic benefit for many, but not all individuals. Autism serves to highlight the critical relationship between the GI tract and neurological/immunological development, in which epigenetic regulation plays a key role. The important role of genetic susceptibility can also be viewed within the context of redox and methylation-related metabolism. This lecture will review the scientific evidence for impaired redox and methylation status in autism, including possible causative factors and implications for treatment.

Learning objectives:
The clinician will:
Learn underlying physiological mechanisms vital to a deeper understanding of autism spectrum disorder
Understand the role of methylation in autism spectrum disorder
Understand the role of oxidative stress and inflammation in autism pathology
Understand the interrelationships of different body systems
Understand epigenetic regulation upon body systems

Richard C. Deth, PhD

Richard Deth, PhD, is Professor of Pharmacology in the Department of Pharmaceutical Sciences, School of Pharmacy, Northeastern University. His recent research has focused on the roles of oxidative stress and impaired methylation in autism, ADHD and other neurological, neuropsychiatric and neurodegenerative disorders.