在帕金森病的细胞和动物模型中，挽救有缺陷的囊泡运输可抵御α-突触核蛋白毒性。

Rescuing defective vesicular trafficking protects against alpha-synuclein toxicity in cellular and animal models of Parkinson's disease.

作者信息

Lashuel Hilal A, Hirling Harald

机构信息

Laboratory of Molecular Neurobiology and Neuroproteomics, Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne, Station 15, CH-1015 Lausanne, Switzerland.

出版信息

ACS Chem Biol. 2006 Aug 22;1(7):420-4. doi: 10.1021/cb600331e.

DOI:10.1021/cb600331e

PMID:17168518

Abstract

Studies in yeast are providing critical insights into the mechanisms of neurodegeneration in Parkinson's disease (PD). A recent study shows that disruption of vesicular trafficking between the endoplasmic reticulum (ER) and the Golgi, caused by the overexpression and/or aggregation of alpha-synuclein, is linked to degeneration of dopamine neurons. Overexpression of proteins that are known to enhance ER-to-Golgi transport rescue defective trafficking in yeast, worm, fly, and cellular models of PD.

摘要

对酵母的研究正在为帕金森病（PD）神经退行性变机制提供关键见解。最近一项研究表明，由α-突触核蛋白的过度表达和/或聚集导致的内质网（ER）与高尔基体之间囊泡运输的破坏与多巴胺能神经元的变性有关。已知增强ER到高尔基体运输的蛋白质的过表达可挽救酵母、蠕虫、果蝇和PD细胞模型中的缺陷运输。