Mitochondria may mediate prenatal environmental influences in autism spectrum disorder

Abstract

We propose that the mitochondrion, an essential cellular organelle, mediates the long-term prenatal environmental effects of disease in autism spectrum disorder (ASD). Many prenatal environmental factors which increase the risk of developing ASD influence mitochondria physiol-ogy, including toxicant exposures, immune activation, and nutritional factors. Unique types of mi-tochondrial dysfunction have been associated with ASD and recent studies have linked prenatal environmental exposures to long‐term changes in mitochondrial physiology in children with ASD. A better understanding of the role of the mitochondria in the etiology of ASD can lead to targeted therapeutics and strategies to potentially prevent the development of ASD.