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.
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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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