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微小RNA375-3p/雷帕霉素通过降低早老素1介导雷帕霉素靶蛋白（mTOR）信号通路，增强小胶质细胞活性以调节阿尔茨海默病中的自噬。

miRNA375-3p/rapamycin mediates the mTOR pathway by decreasing PS1, enhances microglial cell activity to regulate autophagy in Alzheimer's disease.

作者信息

Wang Yuxiang, Xiao Zixuan, Yin Hanlan, Ren Zhichao, Ma Xueting, Wang Yibo, Zhang Yan, Fu Xueqi, Zhang Fuqiang, Zeng Linlin

机构信息

Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Science, Jilin University, Changchun, 130012, China.

Scientific Research Centre of China-Japan Union Hospital, Jilin University, Changchun, 130033, China.

出版信息

Heliyon. 2024 Sep 19;10(19):e37589. doi: 10.1016/j.heliyon.2024.e37589. eCollection 2024 Oct 15.

DOI:10.1016/j.heliyon.2024.e37589
PMID:39386837
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11461998/
Abstract

The clinical prevention, diagnosis, treatment, and drug development of Alzheimer's disease (AD) require urgent detection of novel targets and methods. Autophagy and microglia are significantly associated with the pathogenesis of early AD. This study indicated that microRNA-375-3p can inhibit autophagy by promoting mTOR phosphorylation in normal physiological conditions, while microRNA-375-3p promoted autophagy and enhanced neural repair by inhibiting the expression of presenilin 1 in early AD pathogenesis. Furthermore, co-treatment of rapamycin, and microRNA-375-3p can synergistically promote the autophagy and microglial activation in a neuroprotective manner, clear Aβ accumulation, repair nerve damage, and alleviate cognitive dysfunction and memory defects in APP/PS1 TG mice. This research revealed the impact and mechanism of miR375-3p on the early stage of AD through and experiments and provides new ideas and directions for the early treatment of AD.

摘要

阿尔茨海默病（AD）的临床预防、诊断、治疗及药物研发迫切需要发现新的靶点和方法。自噬和小胶质细胞与早期AD的发病机制密切相关。本研究表明，在正常生理条件下，微小RNA-375-3p可通过促进mTOR磷酸化来抑制自噬，而在早期AD发病机制中，微小RNA-375-3p通过抑制早老素1的表达来促进自噬并增强神经修复。此外，雷帕霉素与微小RNA-375-3p联合处理可协同以神经保护方式促进自噬和小胶质细胞活化，清除Aβ堆积，修复神经损伤，并减轻APP/PS1转基因小鼠的认知功能障碍和记忆缺陷。本研究通过[具体实验]和[具体实验]揭示了miR375-3p对AD早期阶段的影响及其机制，为AD的早期治疗提供了新的思路和方向。

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4
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