What's So Fly About Autism? Investigating the link between Mitochondrial Dysfunction in the Brain and Habituation in the Ube3a Drosophila ASD model

A lack of proper understanding of the pathway or mechanism connecting mitochondrial dysfunction and ASD exists. We propose that looking at mitochondrial dysfunction in relation to these a specific gene implicated in ASD – Ube3a – would help elucidate the pathways involved in ASD. Cellular oxidative stress, a by-product of mitochondrial dysfunction, has been implicated in ASD. Thus, in this research, mitochondrial dysfunction, cellular and mitochondrial oxidative stress in the brain of Ube3a knock down mutants will be explored in Drosophila in relation to habituation which is hypothesized to underlie social impairments in ASD. Additionally antioxidant treatment using 1% vitamin C will be applied in order to ascertain links between habituation and mitochondrial dysfunction. The data suggest that a large portion of the mitochondria in Ube3a mutants are unhealthy as well as higher mitochondrial and cellular oxidative stress compared to WT. Habituation deficits are also observed however application of antioxidant treatment proved to be unaffected in alleviating these deficits.