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 γ-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.