期刊
MOLECULAR NEUROBIOLOGY
卷 46, 期 1, 页码 41-54出版社
SPRINGER
DOI: 10.1007/s12035-012-8246-0
关键词
Alzheimer's disease; Proteostasis; Aging; Chaperones; UPS; Autophagy
资金
- Alzheimer Forschung Initiative e.V. AFI
- Deutsche Forschungsgemeinschaft (DFG) [FOR926]
Alzheimer's disease (AD) is one key medical challenge of the aging society and despite a great amount of effort and a huge collection of acquired data on molecular mechanisms that are associated with the onset and progression of this devastating disorder, no causal therapy is in sight. The two main hypotheses of AD, the amyloid cascade hypothesis and the Tau hypothesis, are still in the focus of AD research. With aging as the accepted main risk factor of the most important non familial and late onset sporadic forms of AD, it is now mandatory to discuss more intensively aspects of cellular aging and aging biochemistry and its impact on neurodegeneration. Since aging is accompanied by changes in cellular protein homeostasis and an increasing demand for protein degradation, aspects of protein folding, misfolding, refolding and, importantly, protein degradation need to be linked to AD pathogenesis. This is the purpose of this short review.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据