UC Davis

Mitochondria are organelles involved in essential roles in intermediary metabolism, perinatal neurodevelopment, immunity, bioenergetics, neurotransmitter metabolism, among other critical pathways. As such, mitochondrial dysfunction (MD) has deleterious effects with the potential of contributing to neurological diseases or enhancing their morbidity (e.g., autism and schizophrenia). Therefore, accumulation of mitochondrial damage is interpreted as a key element of the development of aging as well as neurodegenerative diseases. With the rise in the prevalence of autism spectrum disorders (ASD), there has been an increased interest in the etiology and contributors of this disorder. MD caused by genetics alone or by gene and environment interactions, may play a role in the etiology of ASD and holds promise for developing future therapies and/or interventions to help manage its symptoms or delaying its onset. Here we explore findings from our research and others analyzing the role of mitochondrial DNA damage as a contributor to ASD morbidity.