tau蛋白和β-淀粉样蛋白在阿尔茨海默病病理过程中作用及自噬机制的研究概况

Research situation of tau proteins and β-amyloid protein in the pathological process and autophagic mechanisms in Alzheimer′s disease

阿尔茨海默病(AD)是引起老年痴呆最常见的一种神经退行性疾病。tau蛋白和β-淀粉样蛋白(Aβ)(1-42)的错误折叠和积聚引起进行性神经元丢失。目前观点认为,AD主要的生物学标志tau蛋白和Aβ能够反映其病理特征,即反映神经元外神经元纤维缠结和神经元内老年斑的沉积。自噬是一种高度保守的溶酶体依赖性的降解程序,可以为机体供能、清理代谢废物、平衡免疫炎症反应等。笔者概述tau蛋白和Aβ在AD病理过程中的作用及自噬机制的研究现状。

Alzheimer′s disease(AD) is a neurodegenerative disease which is the most common form of dementia in the elderly. Misfolding and accumulation of tau proteins and β-amyloid (Aβ)(1-42) cause progressive neuronal loss. In recent researches, the biological markers of AD, tau proteins and β-amyloid protein, could reflect its pathological features as including neuronal fiber tangles (NFTs) and senile plaque (SP) deposition in neurons. Autophagy is a highly conserved lysosomal-dependent degradation process that supplies energy to the body, cleans up metabolic waste, and balances immune inflammatory responses.In this review, we concluded the pathology of tau proteins and Aβ protein and the autophagic mechanisms in AD.