Mitochondria may mediate prenatal environmental influences in autism spectrum disorder

Richard E. Frye, Janet Cakir, Shannon Rose, Raymond F. Palmer, Christine Austin, Paul Curtin, Manish Arora

Research output: Contribution to journalReview articlepeer-review

15 Scopus citations


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.

Original languageEnglish (US)
Article number218
JournalJournal of Personalized Medicine
Issue number3
StatePublished - Mar 2021


  • Autism spectrum disorder
  • Immune dysfunction
  • Mitochondria
  • Oxidative stress
  • Prenatal environment

ASJC Scopus subject areas

  • Medicine (miscellaneous)


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