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Evidence of Mitochondrial Dysfunction in Autism: Biochemical Links, Genetic-Based Associations, and Non-Energy-Related Mechanisms - PubMed Skip to main page content
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Review
. 2017:2017:4314025.
doi: 10.1155/2017/4314025. Epub 2017 May 29.

Evidence of Mitochondrial Dysfunction in Autism: Biochemical Links, Genetic-Based Associations, and Non-Energy-Related Mechanisms

Keren K Griffiths  1 , Richard J Levy  1
Affiliations
Review

Evidence of Mitochondrial Dysfunction in Autism: Biochemical Links, Genetic-Based Associations, and Non-Energy-Related Mechanisms

Keren K Griffiths et al. Oxid Med Cell Longev. 2017.

Abstract

Autism spectrum disorder (ASD), the fastest growing developmental disability in the United States, represents a group of neurodevelopmental disorders characterized by impaired social interaction and communication as well as restricted and repetitive behavior. The underlying cause of autism is unknown and therapy is currently limited to targeting behavioral abnormalities. Emerging studies suggest a link between mitochondrial dysfunction and ASD. Here, we review the evidence demonstrating this potential connection. We focus specifically on biochemical links, genetic-based associations, non-energy related mechanisms, and novel therapeutic strategies.

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Figures

Figure 1
Figure 1
Relationship between mitochondrial disease, ASD, and autism. Mitochondrial disease in most children with ASD is of the non-classical variety. Up to 5% of children with autism have classical mitochondrial disease while 10–20% of patients with classic mitochondrial disease demonstrate ASD features. The co-existence of ASD with mitochondrial disease is higher than the prevalence of either ASD or mitochondrial disease in the general population, suggesting a link between mitochondrial dysfunction and autism. Reprinted from [9].
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