The Developmental Neuroscience Laboratory studies the biochemical and immunological changes associated with autism in blood samples, lymphoblast cell cultures, and postmortem brain samples, particularly as they relate to markers of oxidative stress, mitochondrial function, and inflammatory response. We are also studying the relationship, if any, between these abnormalities and low- or high-functioning autism groups, as well as the severity of behavior deficits and neuropathological abnormalities in autism. This study will help identify biochemical and immunological targets for the diagnosis and therapeutic intervention of autism.
Increasing evidence from our laboratory and others suggests the presence of oxidative stress and mitochondrial abnormalities in individuals with autism, and that these individuals’ response and/or inflammatory response may be compromised. We are studying the mechanism of mitochondrial dysfunction in autism and whether the oxidative stress in autism is caused by an increased production of free radicals, deficiencies of anti-oxidants, or both. These free radicals are highly toxic and, if not removed or neutralized, they react with lipids, proteins, and nucleic acids and damage membrane properties and cellular functions. Excessive oxidative damage eventually leads to cell death.
Another area we are investigating is whether diets with walnuts, which are rich in antioxidants and anti-inflammatory components, can attenuate oxidative stress and associated cellular death and improve cognitive and behavioral function in neurological diseases such as Alzheimer disease.