Mitochondrial Dysfunction in Autism

Autism spectrum disorders (ASDs) are neurodevelopmental disorders that cause behavioral, social, and communication impairments. Several lines of evidence from biochemical, anatomical, and neuroradiographical studies suggest impairment of energy metabolism and mitochondrial dysfunction in ASDs. Mitochondrial electron transport chain (ETC) abnormalities result in reduced production of energy, i.e., adenosine triphosphate (ATP), and enhanced generation of free radicals. Mitochondria also play a central role in maintaining intracellular calcium homeostasis. Both mitochondrial DNA and nuclear DNA (nDNA) encode the subunits of ETC complexes. Any mtDNA mutation or deletion can result in deficiency of ETC complexes and, subsequently, in mitochondrial dysfunction. The brain has a high demand for energy that is provided by mitochondria. Here, we review the evidence about mitochondrial dysfunction in autism, including decreased activities and protein expression levels of ETC complexes, mtDNA or nDNA mutations, oxidative stress, and calcium-signaling abnormalities in autism.