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基于Aβ与tau蛋白过度磷酸化损伤机制的阿尔茨海默病治疗靶点
引用本文:林炼峰,罗焕敏.基于Aβ与tau蛋白过度磷酸化损伤机制的阿尔茨海默病治疗靶点[J].神经科学通报,2011,27(1):53-60.
作者姓名:林炼峰  罗焕敏
摘    要:阿尔茨海默病(Alzheimer's disease,AD)的发病机制主要包括Aβ蛋白表达增高在脑内聚集形成老年斑和tau蛋白过度磷酸化在胞内形成神经原纤维缠结.尽管Aβ与tau蛋白的损伤机制一直是AD研究的重点,但目前仍未找到能有效治疗AD的药物.本文主要概述了Aβ蛋白聚集与tau蛋白过度磷酸化对大脑损伤作用的分子机...

关 键 词:阿尔茨海默病  Aβ聚集  tau蛋白过度磷酸化  治疗靶点
收稿时间:2010 Nov 3

Screening of treatment targets for Alzheimer’s disease from the molecular mechanisms of impairment by β-amyloid aggregation and tau hyperphosphorylation
Lian-Feng Lin,Huan-Min Luo.Screening of treatment targets for Alzheimer’s disease from the molecular mechanisms of impairment by β-amyloid aggregation and tau hyperphosphorylation[J].Neuroscience Bulletin,2011,27(1):53-60.
Authors:Lian-Feng Lin  Huan-Min Luo
Institution:1. Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, China
2. Institute of Brain Sciences, Jinan University, Guangzhou, 510632, China
3. The Joint Laboratory of Brain Function and Health, Jinan University and The University of Hong Kong, Jinan University, Guangzhou, 510632, China
Abstract:β-Amyloid (Aβ) over-expression and tau hyperphosphorylation are considered to be the central events in the pathogenesis of Alzheimer’s disease (AD). Studies on them may help elucidate the precise molecular pathogenesis of AD. Until now, although tau protein and Aβ remain the foci of AD research, the etiopathogenesis of AD and effective drugs for AD treatment are still largely unsolved. The present review was mainly focused on the molecular mechanism of Aβ aggregation-related impairment and the pathways leading to tau hyperphosphorylation, based on which some promising therapeutic targets for AD were also proposed.
Keywords:Alzheimer’s disease  Aβ aggregation  tau hyperphosphorylation  treatment targets
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