Department of Pharmacology, School of Medicine, Jinan University, Guangzhou 510632, China.
Neurosci Bull. 2011 Feb;27(1):53-60. doi: 10.1007/s12264-011-1040-6.
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.
β-淀粉样蛋白（Aβ）过度表达和 tau 过度磷酸化被认为是阿尔茨海默病（AD）发病机制中的核心事件。对它们的研究可能有助于阐明 AD 的精确分子发病机制。到目前为止，尽管 tau 蛋白和 Aβ仍然是 AD 研究的焦点，但 AD 的病因发病机制和有效的 AD 治疗药物仍在很大程度上尚未解决。本综述主要集中在 Aβ聚集相关损伤的分子机制和导致 tau 过度磷酸化的途径上，并在此基础上提出了一些有希望的 AD 治疗靶点。
