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.
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制, 并从中寻找治疗AD的潜在靶点, 有助于阐明AD发病机理以及寻找有效的AD治疗药物。