What is it about?

Previous studies of postmortem brains or peripheral samples have suggested a role of mitochondrial dysfunction in the pathophysiology of autism spectrum disorder. The current case-control positron emission tomography study demonstrated the significantly low mitochondrial electron transport chain complex I availability in anterior cingulate cortex of psychotropics-free participants with high-functioning autism spectrum disorder compared with age-, sex-, parental socioeconomical status-, and intelligence level-matched typically developed controls, and further revealed their significant correlations with severe sociocommunicational autism core symptom.

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Why is it important?

The present study provided the first and direct in vivo human brain evidence linking mitochondrial dysfunction to the core feature of autism spectrum disorder.


Our current study provides direct evidence to link in vivo brain mitochondrial dysfunction with ASD pathophysiology and its communicational deficits. Our findings support the possibility that mitochondrial electron transport chain complex I is a novel therapeutic target for ASD core symptoms.

Hidenori Yamasue
Hamamatsu University School of Medicine

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This page is a summary of: Lower Availability of Mitochondrial Complex I in Anterior Cingulate Cortex in Autism: A Positron Emission Tomography Study, American Journal of Psychiatry, September 2022, American Psychiatric Association,
DOI: 10.1176/appi.ajp.22010014.
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