Protein misfolding, amyloid formation, and neurodegeneration: A critical role for molecular chaperones?

被引：230

作者：

Muchowskil, PJ ^{[1
]}

机构：

[1] Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA

来源：

NEURON | 2002年 / 35卷 / 01期

关键词：

D O I：

10.1016/S0896-6273(02)00761-4

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The most conspicuous feature of many neurodegenerative disorders, including Alzheimer's, Parkinson's, and Huntington's disease, is the occurrence of protein aggregates in ordered fibrillar structures known as amyloid found inside and outside of brain cells. The appearance of aggregates in diseased brains implies an underlying incapacity in the cellular machinery of molecular chaperones that normally functions to prevent the accumulation of misfolded proteins. Here we review recent studies that have revealed a critical role for molecular chaperones in several neurodegenerative disorders.

引用

页码：9 / 12

页数：4

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