During the study data from autistic children aged 2 to 5 years was thoroughly scrutinized. Authors analyzed mitochondrial dysfunction and mitochondrial DNA (mtDNA) abnormalities in lymphocytes from 10 children with autism and 10 controls. It appeared that mitochondrial-dependent oxygen consumption was impaired in peripheral blood lymphocytes from autistic kids than control children. Lymphocytic mitochondria in autism supposedly had a lower oxidative phosphorylation.
Scientists enlighten, “The high prevalence of mitochondrial dysfunction observed in this preliminary study performed with children presenting with full syndrome autism may or may not indicate an etiological [causal] role. Whether the mitochondrial dysfunction in children with autism is primary or secondary to an as-yet unknown event remains the subject of future work; however, mitochondrial dysfunction could greatly amplify and propagate brain dysfunction, such as that found in autism, given that the highest levels of mtDNA abnormalities are observed in postmitotic [a mature cell that is no longer capable of undergoing mitosis (cell division)] tissues with high energy demands (e.g., brain).”
While mitochondrial DNA over replication was registered in 5 patients, deletions were witnessed in 2 patients. Cecilia Giulivi, Ph.D., of the University of California, Davis, and colleagues claim that children with full syndrome autism have mitochondrial dysfunction. Additional investigations can be carried out to lay
The study is published in the December 1 issue of JAMA.