SIRT4 promotes neuronal apoptosis in models of Alzheimer’s disease via the STAT2–SIRT4–mTOR pathway

Author:

Xing Dianxia12,Zhang Wenjin3,Cui Wei3,Yao Xiuya3,Xiao Yaping4,Chen Lihua1,Yuan Shiyun1,Duan Yanyan5,Yu Weihua6,Pan Pengfei7,Lü Yang1ORCID

Affiliation:

1. Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China

2. Department of Geriatrics, Chongqing University Three Gorges Hospital, Chongqing, China

3. Central Laboratory of Chongqing University Three Gorges Hospital, Chongqing, China

4. Department of Pharmacy and Pharmacology, Chongqing University Three Gorges Hospital, Chongqing, China

5. College of Biology and Food Engineering, Chongqing Three Gorges University, Chongqing, China

6. Institute of Neuroscience, Chongqing Medical University, Chongqing, China

7. Intensive Care Unit, Chongqing University Three Gorges Hospital, Chongqing, China

Abstract

The study reveals that in Alzheimer’s disease models, SIRT4 expression increases, contributing to neuronal apoptosis and amyloid-β deposition. Reducing SIRT4 lessens apoptosis and amyloid-β accumulation, improving memory in mice. This process involves the mTOR pathway, regulated by STAT2 transcription factor. These findings suggest targeting the STAT2-SIRT4-mTOR axis as a potential Alzheimer’s treatment strategy.

Funder

Science and Technology Bureau of Wanzhou, Chongqing

CSTC | Chongqing Science and Technology Foundation

Chongqing Municipal Education Commission

Fundamental Research Funds for the Key Research Program of Chongqing Science and Technology Commission

Science and Technology Bureau of Wanzhou District, Chongqing

Publisher

American Physiological Society

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