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TUESDAY, Nov. 30 (HealthDay News) -- Children with autism may be more likely to have impaired mitochondrial function and abnormalities in mitochondrial DNA (mtDNA) than children without autism, according to preliminary research published in the Dec. 1 issue of the Journal of the American Medical Association.
Cecilia Giulivi, Ph.D., of the University of California at Davis, and colleagues evaluated mitochondrial dysfunction and mtDNA abnormalities using lymphocytes from 10 children with autism, aged 2 to 5 years, matched to 10 controls.
The researchers noted impaired mitochondrial-dependent oxygen consumption in the peripheral blood lymphocytes from children with autism; the patient group's lymphocytic mitochondria also displayed a reduction in oxidative phosphorylation capacity, which contributes to increased cellular oxidative stress. Five patients showed mtDNA overreplication, and two showed deletions.
"In this preliminary study, evidence of mitochondrial dysfunction was observed in children presenting with full syndrome autism. More research is needed to understand the molecular causes of the mitochondrial dysfunction and how this and other neurometabolic defects may contribute to autism or related phenotypes," the authors write.
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