Mitochondria: A Common Target for Genetic Mutations and Environmental Toxicants in Parkinson's Disease.

Mitochondria: A Common Target for Genetic Mutations and Environmental Toxicants in Parkinson's Disease.
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DOI:
10.3389/fgene.2017.00177
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发表时间:
2017
影响因子:
3.7
通讯作者:
Tieu K
Tieu K
中科院分区:
生物学3区
文献类型:
--
作者:
Helley MP;Pinnell J;Sportelli C;Tieu K

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帕金森病(PD)是一种毁灭性的神经运动障碍。自200年前首次发现以来,遗传和环境因素已被确定在PD的发生和进展中发挥作用。虽然在过去的几十年里,基因研究一直是PD研究的主要推动力,但目前只有一小部分PD病例可以直接与单基因突变联系起来。其余病例归因于其他风险相关基因、环境暴露和基因-环境相互作用,使PD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经对帕金森病的发病机制和潜在的治疗靶点产生了重要的见解。这篇综述将强调线粒体功能障碍是与帕金森病相关的基因突变和环境毒物的共同途径。
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.
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