Alzheimer's disease (AD) is a neurodegeneration csharacterized by
amyloid-β (Aβ) deposition and abnormally phosphorylated
Tau protein aggregation. Autophagy, as an important cellular metabolic activity, is closely related to the production, secretion and clearance of Aβ
peptide and Tau phosphorylation level. Therefore, autophagy may become a potential target for AD treatment. A large number of molecules are involved in the
mammalian target of rapamycin (mTOR)-dependent or mTOR-independent pathway of autophagy. More and more evidences show that
statins can intervene autophagy by regulating the activity or expression level of
autophagy-related proteins and genes. On the one hand,
statins can induce autophagy through Sirtuin1 (
SIRT1), P21, nuclear P53 and adenylate activated
protein kinase (AMPK). On the other hand,
statins inhibit the
mevalonate metabolism pathway, thereby interfering with the prenylation of
small GTPases, leading to autophagy dysfunction.
Statins can also reduce the levels of LAMP2 and
dynein, destroying autophagy. In this review, we focused on the role of autophagy in AD and the autophagy mechanism of
statins in the potential treatment of AD.