Mitochondrial Dysfunction in Children with Autism
Isaac Pessah, Ph.D., and Irva Hertz-Picciotto, M.P.H., Ph.D
NIEHS Grants P01ES011269 and R01ES015359
Children with autism are far more likely to have deficits in mitochondrial function, specifically in their ability to produce cellular energy, than are typically developing children. These findings are from a new study by NIEHS-supported researchers at the University of California Davis. The results suggest that cumulative damage and oxidative stress in mitochondria could influence both the onset and severity of autism.
The brain is the second largest consumer of energy in the body after the heart. The investigators propose that deficiencies in the ability to fuel brain cells might lead to some of the cognitive impairments associated with autism. Mitochondrial dysfunction has already been associated with other neurological diseases and conditions included Parkinson's and Alzheimer's disease, schizophrenia, and bipolar disorder.
Although the study was small including only ten children with autism and ten age-matched controls, the findings may eventually help physicians provide early diagnosis. Larger studies are necessary to confirm these findings. The study does not identify the cause of autism which affects as many as one in every 110 children, but it does offer new insights into prevention and intervention efforts.
Citation: Giulivi C, Zhang YF, Omanska-Klusek A, Ross-Inta C, Wong S, Hertz-Picciotto I,Tassone F, Pessah IN. Mitochondrial dysfunction in autism. JAMA. 2010 Dec 1;304(21):2389-96.
Mitochondrial, but not Nuclear Ligase3 is Required for Cellular Viability