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Children with autism have mitochondrial dysfunction |
A study led by Cecilia Giulivi, professor in the Department of Molecular Biosciences in the School of Veterinary Medicine at University of California Davis Medical Centre shows that children with autism are likely to have malfunctioning mitochondria. Mitochondria are the primary source of energy production in cells and have their own genetic instruction to carry out aerobic respiration. Oxidative stress and cumulative damage in the mitochondria could influence both the onset and severity of autism which suggests a clear link between autism and mitochondrial defects. The symptoms of mitochondrial dysfunction can be seen in such neurological conditions as Parkinson’s, Alzheimer’s, Schizophrenia and bipolar disorder, and the authors of this study propose that deficiencies in the ability to fuel brain neurons might lead to some of the cognitive impairments associated with autism. Ten autistic children aged two to five years from the same background were recruited for the study. The metabolic pathways of mitochondria in immune cells called lymphocytes were analysed, and the researchers found that the mitochondria from autistic children consumed far less oxygen than those from the control group of children. In one critical enzyme complex the oxygen consumption of the autistic group was one third of that from the control group. Reduced function was widespread amongst the autistic children, and levels of pyruvate, the raw material that mitochondria transform into cellular energy was higher in the blood plasma of autistic children suggesting that they are unable to process the pyruvate fast enough to keep up with demand for energy. This in turn points to a deficiency in the enzyme pyruvate dehydrogenase. Due to the high levels of hydrogen peroxide in autistic children Giuvili concluded that the cells of these children would be more vulnerable to oxidative stress as they would be unable to repair the damage caused by free radicals. These results imply that these abnormalities, defects and levels of malfunction could be influencing autism’s onset, but they do not confirm any cause of autism, Giuvili cautions. Whether these abnormalities took place before or after the children were born the researchers are unable to say. But the results would allow for an earlier diagnosis of autism than previously possible, and physicians need to be made aware of these results. The study also refines the search for autism’s origins. Giuvili and her team are now looking at the mitochondrial DNA for more clues of the precise differences between children with and without autism. If they can understand the role of mitochondrial dysfunction in children with autism, and exposure to the environmental stressors that caused the damage, it may help to explain the range of symptoms of autism. Additional research in this area could possibly lead to prevention or intervention efforts in the development of autism. Journal of the American Medical Association First published in November 2010 |
