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淀粉样蛋白毒性蛋白的线粒体降解——神经退行性疾病的新视角。

Mitochondrial degradation of amyloidogenic proteins - A new perspective for neurodegenerative diseases.

机构信息

Molecular Neuroscience Group, Department of Chemical Engineering and Biotechnology, University of Cambridge, West Cambridge Site, Philippa Fawcett Drive, Cambridge, CB3 0AS, UK.

Molecular Neuroscience Group, Department of Chemical Engineering and Biotechnology, University of Cambridge, West Cambridge Site, Philippa Fawcett Drive, Cambridge, CB3 0AS, UK.

出版信息

Prog Neurobiol. 2019 Oct;181:101660. doi: 10.1016/j.pneurobio.2019.101660. Epub 2019 Jul 10.

Abstract

This perspective article outlines mechanisms of mitochondrial import and protein degradation and how these have been linked to alpha-synuclein and Amyloid beta (Aβ) homeostasis. Our aim is to underpin and stimulate the debate on the recent conception of mitochondria as protein degrading organelles, which suggests that mitochondria are more directly involved in neurodegenerative diseases than previously assumed.

摘要

这篇观点文章概述了线粒体的输入和蛋白质降解的机制,以及它们如何与α-突触核蛋白和淀粉样β(Aβ)的动态平衡相关联。我们的目的是支持并激发关于线粒体作为蛋白质降解细胞器的最新概念的辩论,该概念表明线粒体比以前认为的更直接参与神经退行性疾病。

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