中文摘要：

细胞自噬是生物体内一种用于清除功能异常的细胞器、错误折叠的蛋白质、被氧化的脂类等有害大分子物质的重要途径.它的机制从低等生物酵母到高等的哺乳动物都高度保守,对维持正常的生命活动至关重要.错误折叠的蛋白质若不能被有效清除,就会造成积聚,致使神经细胞功能丧失乃至死亡,这是神经退行性疾病包括老年性痴呆（Alzheimer＇s disease,AD）的主要原因.本文回顾了近年来关于细胞自噬及其与老年性痴呆关系的研究进展,主要内容包括以下几点：自噬参与Aβ的产生和清除;γ分泌酶中的Presenilin 1在自噬底物降解中的作用;Tau蛋白调控自噬体转运、融合;老年性痴呆早期自噬对细胞的保护;细胞中感应营养和能量的两个关键蛋白mTOR和AMPK调控自噬及其对老年性痴呆的潜在影响机制.

英文摘要：

Autophagy is a main pathway that clears the dysfunction organelles, misfolding proteins and oxidative lipids. It＇s important for maintaining life activity and conserved from yeast to mammalian. In the AD neurons the misfolding proteins were not efficiently cleared then accumulated. These caused neurons loss of function even neuron death. This review focuses on the recent progresses on regulation of autophagy and the role of autophagy in Alzheimer＇s diseases. Autophagy is protective in early stage of AD, although it induces autophagic cell death in late stage of AD. Autophagosome may be the main site for Aβ production and clearance. Presenilin 1 which is the key proteinase in β-secrectase also plays a role in lysosomal acidification which is a key step for autophagic degradation. Tau may be involved in autophagosome trafficking and autophagosome-lysosome fusion, mTOR and AMPK sensing nutrients and energy in cells also regulate autophagy.