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Mitochondrial Dysfunction in Autism and Attention-Deficit/Hyperactivity Disorder: Evidence from Genetic, Biochemical,
Tina R Ram1,2, Chunlong Mu2,3,4, Sarah J MacEachern2,3,5
1Department of Biochemistry and Molecular Biology, Cumming School of Medicine, Faculty of Kinesiology, University of Calgary, Calgary, AB T2N 4N1, Canada.
Antioxidants (Basel, Switzerland)
|June 26, 2026
Summary
Mitochondrial dysfunction is a key factor in autism and ADHD. Impaired energy production and increased oxidative stress in the brain are linked to these neurodevelopmental conditions.
Area of Science:
- Neuroscience
- Biochemistry
- Genetics
Background:
- Mitochondrial dysfunction is increasingly linked to neurodevelopmental conditions like autism and ADHD.
- The developing brain's reliance on ATP production makes it vulnerable to impairments in oxidative phosphorylation and mitochondrial dynamics.
Purpose of the Study:
- To review evidence characterizing mitochondrial impairment in autism and ADHD.
- To explore the role of mitochondrial dysfunction as a transdiagnostic feature.
Main Methods:
- Review of postmortem neurochemistry, genomics, and biomarker research.
- Analysis of in vivo neuroimaging studies (magnetic resonance spectroscopy).
Main Results:
- Autism studies show elevated mitochondrial DNA variants, altered respiratory chain complexes (I, III, V), and increased oxidative stress.
- Neuroimaging reveals elevated cerebral lactate and reduced phosphocreatine-to-ATP ratios in vivo.
- ADHD evidence, though limited, also suggests mitochondrial involvement.
Conclusions:
- Mitochondrial dysfunction is a transdiagnostic biological feature in neurodevelopmental conditions.
- Findings support potential for mechanistic biomarker identification and targeted therapeutic development.
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