Mitochondrial Dysfunction and Its Relationship with mTOR Signaling and Oxidative Damage in Autism Spectrum Disorders

摘要: Mitochondria are organelles that play a central role in processes related to cellular viability, such as energy production, cell growth, death via apoptosis, and metabolism of reactive oxygen species (ROS). We can observe behavioral abnormalities relevant autism spectrum disorders (ASDs) their recovery mediated by the mTOR inhibitor rapamycin mouse models. In Tsc2 +/- mice, transcription multiple genes involved signaling is enhanced, suggesting crucial of dysregulated ASD model. This review proposes may be useful for the pharmacological treatment ASD. offers novel insights into mitochondrial dysfunction related impaired glutathione synthesis lower detoxification capacity. Firstly, children with concomitant mitochondrial have been reported manifest clinical symptoms similar those disorders, and it therefore shows manifestations concomitant diagnosis dysfunction are likely due these disorders. Secondly, adenosine triphosphate (ATP) production/oxygen consumption pathway potential candidate preventing oxidative stress, and disruption ATP alone impaired synthesis. Finally, decrease total antioxidant capacity account who show core social impairments without neurological and somatic symptoms.