Alzheimer’s disease (AD) is a neurodegeneration csharacterized by
amyloid- (A) deposition and abnormally phosphorylated Tau
protein aggregation. Autophagy, as an important cellular metabolic activity, is
closely related to the production, secretion and clearance of A 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.