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Mitochondrial Dysfunction May Be Important Biomarker for ADHD, ASD
Researchers have identified a “significant relationship” between higher mitochondrial DNA copy number (mtDNA-cn) and the occurrence of attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Results from the systematic review and meta-analysis were published in the journal Frontiers in Psychiatry.
“In previous studies, both increased and decreased mtDNA-cn in blood and other tissues have been linked to neurodevelopmental disorders, suggesting a diverse and complicated role of altered mtDNA-cn in these disorders,” the authors wrote in the study discussion. “In this study, we performed a meta-analysis to summarize the current evidence and to provide more conclusive results regarding the relationship between mtDNA-cn and ASD/ADHD.”
Researchers identified 14 studies in the MEDLINE-PubMed, Scopus, and EMBASE databases that encompass 666 cases of ADHD and ASD, and 585 controls. Seeking a more precise assessment of the mtDNA-cn in ADHD and ASD, the authors pooled results through random effects meta-analysis, reported as a geometric mean of the estimated average response ratio and 95% confidence interval.
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Overall analysis revealed differences in mtDNA-cn in blood samples (k=10) and brain tissue and oral samples (k=4), which suggests significantly higher mtDNA-cn in patients with ADHD/ASD compared to controls (p=0.0275). Analysis stratified according to tissue type exhibited no significant increase in mtDNA-cn in blood samples between patients and controls (p=0.284), while higher mtDNA-cn was found in non-blood samples in patients than in controls (p=0.0122).
Stratification based on blood-cell composition (p=0.074) as well as age-matching for blood samples (p=0.214) revealed no significant differences between patients and controls. In age-matched non-blood samples, however, researchers identified a significant increase in mtDNA-cn between patients and controls (p<0.001). Finally, analysis with age-matching and stratification between ADHD and ASD showed no significant difference in mtDNA-cn between patients with ASD and controls (p=0.385), whereas there was a significant increase in mtDNA-cn between patients with ADHD and controls (p=0.033).
“In this first meta-analysis of the evaluation of mtDNA-cn in ASD/ADHD, our results show elevated mtDNA-cn in ASD and ADHD, further emphasizing the implication of mitochondrial dysfunction in neurodevelopmental disorders,” the authors wrote in the study conclusion. “However, our results indicate that the mtDNA-cn in blood is not reflected in other tissues in ASD/ADHD, and the true relationship between blood-derived mtDNA-cn and ASD/ADHD remains to be defined in future studies.”
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