Protein homeostasis, aging and Alzheimer's disease.
Protein homeostasis, aging and Alzheimer's disease.
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DOI：
10.1007/s12035-012-8246-0
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发表时间：
2012-08
影响因子：
5.1
通讯作者：
Behl, Christian
中科院分区：
文献类型：
--
作者：
Morawe, Tobias;Hiebel, Christof;Kern, Andreas;Behl, Christian
阿尔茨海默病（AD）是老龄化社会的一个关键医学挑战，尽管对这种毁灭性疾病的发病和发展相关的分子机制进行了大量的努力和收集了大量的已获得的数据，但目前尚无因果治疗方法。淀粉样蛋白级联假说和Tau蛋白假说是目前阿尔茨海默病研究的两个主要假说。随着衰老被公认为最重要的非家族性和晚发散发性AD的主要危险因素，现在有必要更深入地讨论细胞衰老和衰老生物化学及其对神经退行性疾病的影响。由于衰老伴随着细胞蛋白质稳态的改变和蛋白质降解需求的增加，蛋白质折叠、错误折叠、再折叠以及重要的蛋白质降解等方面需要与AD的发病机制联系起来。这就是这篇简短综述的目的。
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.
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