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微竞争与潜伏病毒如何导致α-突触核蛋白聚集、线粒体功能障碍,最终导致帕金森病。

How microcompetition with latent viruses can cause α synuclein aggregation, mitochondrial dysfunction, and eventually Parkinson's disease.

机构信息

The Center for the Biology of Chronic Disease (CBCD), 3 Germay Dr, Wilmington, DE, 19804, USA.

出版信息

J Neurovirol. 2021 Feb;27(1):52-57. doi: 10.1007/s13365-020-00929-x. Epub 2021 Jan 6.

Abstract

The cause of most Parkinson's disease cases is unknown. However, it is well documented that mitochondrial dysfunction and misfolded α synuclein aggregation are important cellular abnormalities associated with the disease. In this paper, we use the microcompetition model to show how latent viruses, which infect the central and peripheral nervous systems, can cause the observed mitochondrial dysfunction and excess α synuclein aggregation, and eventually, Parkinson's disease.

摘要

大多数帕金森病病例的病因尚不清楚。然而,有大量文献记载表明,线粒体功能障碍和错误折叠的α-突触核蛋白聚集是与该疾病相关的重要细胞异常。在本文中,我们使用微竞争模型来展示潜伏病毒(感染中枢和外周神经系统)如何导致观察到的线粒体功能障碍和过量的α-突触核蛋白聚集,并最终导致帕金森病。

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