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自闭症中线粒体功能障碍的证据:生化联系、基于遗传的关联及非能量相关机制

Evidence of Mitochondrial Dysfunction in Autism: Biochemical Links, Genetic-Based Associations, and Non-Energy-Related Mechanisms.

作者信息

Griffiths Keren K, Levy Richard J

机构信息

Department of Anesthesiology, Columbia University Medical Center, New York, NY, USA.

出版信息

Oxid Med Cell Longev. 2017;2017:4314025. doi: 10.1155/2017/4314025. Epub 2017 May 29.

Abstract

Autism spectrum disorder (ASD), the fastest growing developmental disability in the United States, represents a group of neurodevelopmental disorders characterized by impaired social interaction and communication as well as restricted and repetitive behavior. The underlying cause of autism is unknown and therapy is currently limited to targeting behavioral abnormalities. Emerging studies suggest a link between mitochondrial dysfunction and ASD. Here, we review the evidence demonstrating this potential connection. We focus specifically on biochemical links, genetic-based associations, non-energy related mechanisms, and novel therapeutic strategies.

摘要

自闭症谱系障碍(ASD)是美国增长最快的发育障碍,它代表了一组神经发育障碍,其特征为社交互动和沟通受损以及行为受限和重复。自闭症的根本原因尚不清楚,目前的治疗仅限于针对行为异常。新兴研究表明线粒体功能障碍与ASD之间存在联系。在此,我们综述证明这种潜在联系的证据。我们特别关注生化联系、基于基因的关联、非能量相关机制和新型治疗策略。

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