Has the amyloid cascade hypothesis for Alzheimer's disease been proved?
Has the amyloid cascade hypothesis for Alzheimer's disease been proved?
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DOI：
10.2174/156720506775697098
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发表时间：
2006-02-01
影响因子：
2.1
通讯作者：
Hardy, John
中科院分区：
文献类型：
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作者：
Hardy, John
在对淀粉样蛋白在阿尔茨海默病（AD）中的作用进行了大量的争论之后，淀粉样蛋白前体蛋白（APP）的突变和增加42个残基的淀粉样蛋白B肽（A β 42）水平的加工途径已经确定这些蛋白的功能缺陷或加工是AD发病机制的原因。鉴于Ab42聚集体的神经毒性，该肽在AD发病机制中的中心作用是不言而喻的。在这篇文章中，我总结了支持淀粉样蛋白级联假说的主要证据，并指出其局限性。
After much initial debate for and against tile role of amyloid in Alzheimer's disease (AD), mutations on the amyloid precursor protein (APP) and processing pathways that increase levels of the amyloid b peptide of 42 residues (A beta 42) have established that faulty function or processing of these proteins are responsible for AD pathogenesis. Given the neurotoxicity of aggregates of Ab42, tile central role of this peptide in AD pathogenesis is self evident. In this article, I summarize the major pieces of evidence adduced to support the amyloid cascade hypothesis and point out their limitations.