Helley Martin P, Pinnell Jennifer, Sportelli Carolina, Tieu Kim
Department of Environmental Health Sciences, Florida International University, Miami, FL, United States.
Peninsula Schools of Medicine and Dentistry, Plymouth University, Plymouth, United Kingdom.
Front Genet. 2017 Nov 17;8:177. doi: 10.3389/fgene.2017.00177. eCollection 2017.
Parkinson's disease (PD) is a devastating neurological movement disorder. Since its first discovery 200 years ago, genetic and environmental factors have been identified to play a role in PD development and progression. Although genetic studies have been the predominant driving force in PD research over the last few decades, currently only a small fraction of PD cases can be directly linked to monogenic mutations. The remaining cases have been attributed to other risk associated genes, environmental exposures and gene-environment interactions, making PD a multifactorial disorder with a complex etiology. However, enormous efforts from global research have yielded significant insights into pathogenic mechanisms and potential therapeutic targets for PD. This review will highlight mitochondrial dysfunction as a common pathway involved in both genetic mutations and environmental toxicants linked to PD.
帕金森病（PD）是一种具有破坏性的神经运动障碍。自200年前首次发现以来，已确定遗传和环境因素在帕金森病的发生和发展中起作用。尽管在过去几十年中，基因研究一直是帕金森病研究的主要驱动力，但目前只有一小部分帕金森病病例可直接与单基因突变相关联。其余病例则归因于其他风险相关基因、环境暴露以及基因-环境相互作用，这使得帕金森病成为一种病因复杂的多因素疾病。然而，全球研究的巨大努力已对帕金森病的致病机制和潜在治疗靶点有了重要见解。本综述将重点介绍线粒体功能障碍，这是与帕金森病相关的基因突变和环境毒物所共有的一条通路。
