Abstract

Event Abstract Back to Event Impaired activity of monoamine oxidase A in the brain of children with autism Ved Chauhan1*, Feng Gu1 and Abha Chauhan1 1 NYS Institute for Basic Research in Developmental Disabilities, Department of Neurochemistry, United States Autism is a neurodevelopmental disorder characterized by abnormal social and behavioral abnormalities. Extensive evidence from our and other groups has suggested oxidative stress and mitochondrial dysfunction in autism. Monoamine oxidase A (MAOA), a mitochondrial-bound enzyme, catalyzes the oxidation of endogenous amine-containing neurotransmitters such as serotonin and norepinephrine. The role of MAOA in autism is of particular interest because this enzyme affects the levels of serotonin, which are known to be abnormal in some individuals with autism. In comparison to other alleles of MAOA, the 3-repeat allele is associated with reduced transcription and therefore, reduced activity of MAOA. A few studies have reported an association of the low-activity, 3-repeat MAOA-uVNTR allele with autism. In this study, we analyzed the MAOA activity in the cerebellum and frontal cortex from autistic subjects and age-matched control subjects. In the cerebellum, the activity of MAOA was significantly lower in autism than in control subjects. When the subjects were divided into two subgroups according to their ages: children (ages 4-12 years) and adults (ages 13-38 years), a significant decrease in the activity of MAOA in cerebellum was observed in only children with autism but not in adult autistic group. In the frontal cortex, the MAOA activity in autistic children group was also reduced by 30% than in controls, but there was no significant difference. These results suggest that the brain MAOA activity is lower in autistic children than in control subjects. Lower MAOA activity will cause increase in the levels of related neurotransmitters, such as serotonin, which is one of the most important neurotransmitters influencing behavior and has been reported to have critical relationship with autism. Keywords: Cerebellum, autism, enzyme, frontal cortex, Monoamine oxidase A Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Poster Presentation Session Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Chauhan V, Gu F and Chauhan A (2016). Impaired activity of monoamine oxidase A in the brain of children with autism. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00168 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Prof. Ved Chauhan, NYS Institute for Basic Research in Developmental Disabilities, Department of Neurochemistry, Staten Island, New York, United States, ved.chauhan@opwdd.ny.gov Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ved Chauhan Feng Gu Abha Chauhan Google Ved Chauhan Feng Gu Abha Chauhan Google Scholar Ved Chauhan Feng Gu Abha Chauhan PubMed Ved Chauhan Feng Gu Abha Chauhan Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

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