Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder

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 physiology, including toxicant exposures, immune activation, and nutritional factors. Unique types of mitochondrial 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.

Automated summary

The mitochondrion plays a crucial role in the development of autism spectrum disorder (ASD), with many prenatal environmental factors affecting mitochondrial function. Research has linked prenatal environmental exposures to long-term changes in mitochondrial physiology in children with ASD. Understanding the role of mitochondria in the etiology of ASD can lead to targeted therapeutics and strategies for prevention.