IMR Press / JIN / Volume 21 / Issue 2 / DOI: 10.31083/j.jin2102046
Open Access Review
A review of autophagy mechanism of statins in the potential therapy of Alzheimer’s disease
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1 Department of Neurology, The Affiliated WuXi NO. 2 People’s Hospital of Nanjing Medical University, 214000 Wuxi, Jiangsu, China
*Correspondence: (Tao Ma)
Academic Editors: Giovanna Zamboni and Hongmin Wang
J. Integr. Neurosci. 2022, 21(2), 46;
Submitted: 16 June 2021 | Revised: 27 August 2021 | Accepted: 24 September 2021 | Published: 18 March 2022
Copyright: © 2022 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

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.

Alzheimer's disease
Tau protein
Autophagy flux
Mevalonate pathway
Fig. 1.
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