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Review
. 2021 Mar 18;11(3):218.
doi: 10.3390/jpm11030218.

Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder

Richard E Frye  1 , Janet Cakir  2 , Shannon Rose  3 , Raymond F Palmer  4 , Christine Austin  5 , Paul Curtin  5 , Manish Arora  5
Affiliations
Review

Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder

Richard E Frye et al. J Pers Med. .

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 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.

Keywords: autism spectrum disorder; immune dysfunction; mitochondria; oxidative stress; prenatal environment.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The mitochondria can be negatively affected by many environmental and biological factors associated with autism spectrum disorder (left orange panel) and has many critical roles in cellular physiology (right blue panel). ETC: electron transport chain; DAMP: damage-associated molecular pattern
Figure 2
Figure 2
Self-perpetuating destructive cycles which can result in mitochondrial dysfunction.
See this image and copyright information in PMC

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