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帕金森病发病机制中的年龄-环境与基因-环境相互作用

Age-environment and gene-environment interactions in the pathogenesis of Parkinson's disease.

作者信息

Le Couteur David G, Muller Michael, Yang Maria C, Mellick George D, McLean Allan J

机构信息

Centre for Education and Research on Ageing and the Anzac Research Institute, University of Sydney, Concord RG Hospital, NSW, Australia.

出版信息

Rev Environ Health. 2002 Jan-Mar;17(1):51-64. doi: 10.1515/reveh.2002.17.1.51.

Abstract

Parkinson's disease (PD) is a common neurodegenerative disease characterized by dopaminergic cell death and deposition of Lewy bodies within the substantia nigra of the midbrain. Although the major risk factors for PD are aging and environmental factors, there is an important genetic component. An age-related change in xenobiotic metabolism alters the metabolism of and net exposure to, environmental neurotoxins. Genetic variability in xenobiotic metabolism may similarly increase the susceptibility to PD by altering the metabolism of neurotoxins. Genetic studies of rare familial cases of PD indicate a central mechanistic role for the aggregation of alpha-synuclein, a protein found in Lewy bodies. Environmental factors like pesticides and heavy metals can also influence alpha-synuclein aggregation. Common final pathways for aging, environmental, and genetic mechanisms can thus exist, involving both direct neurotoxicity and alpha-synuclein aggregation.

摘要

帕金森病(PD)是一种常见的神经退行性疾病,其特征是多巴胺能细胞死亡以及中脑黑质内路易小体的沉积。尽管PD的主要风险因素是衰老和环境因素,但也存在重要的遗传因素。外源性物质代谢的年龄相关变化会改变环境神经毒素的代谢及净暴露量。外源性物质代谢的基因变异性可能同样会通过改变神经毒素的代谢而增加患PD的易感性。对罕见家族性PD病例的遗传学研究表明,α-突触核蛋白(一种存在于路易小体中的蛋白质)的聚集起核心机制作用。农药和重金属等环境因素也会影响α-突触核蛋白的聚集。因此,衰老、环境和遗传机制可能存在共同的最终途径,包括直接神经毒性和α-突触核蛋白聚集。

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