Advances in the pathogenesis of Alzheimer's disease: a re-evaluation of amyloid cascade hypothesis.
Advances in the pathogenesis of Alzheimer's disease: a re-evaluation of amyloid cascade hypothesis.
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阿尔茨海默病发病机制的进展：淀粉样蛋白级联假说的重新评估
DOI：
10.1186/2047-9158-1-18
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发表时间：
2012-09-21
影响因子：
12.6
通讯作者：
Zhao Z
中科院分区：
文献类型：
--
作者：
Dong S;Duan Y;Hu Y;Zhao Z
阿尔茨海默病（AD）是一种常见的神经退行性疾病，临床表现为记忆力进行性恶化，病理表现为细胞外淀粉样β (a - β)肽沉积形成老年斑（SP）和大脑中过度磷酸化的tau细胞内神经原纤维缠结（NFT）的组织病理学改变。本文综述了淀粉样蛋白级联假说的最新进展，详细介绍了a- β的产生、代谢和清除，以及一些重要的a- β相关基因在AD病理过程中的关键作用。并对该病的遗传学、神经病理学及发病机制等方面的最新研究进展进行了讨论。
Alzheimer’s disease (AD) is a common neurodegenerative disease characterized clinically by progressive deterioration of memory, and pathologically by histopathological changes including extracellular deposits of amyloid-beta (A-beta) peptides forming senile plaques (SP) and the intracellular neurofibrillary tangles (NFT) of hyperphosphorylated tau in the brain. This review focused on the new developments of amyloid cascade hypothesis with details on the production, metabolism and clearance of A-beta, and the key roles of some important A-beta-related genes in the pathological processes of AD. The most recent research advances in genetics, neuropathology and pathogenesis of the disease were also discussed.