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Neurosci Lett. 2017 Nov 20;661:57-62. doi: 10.1016/j.neulet.2017.09.043. Epub 2017 Sep 22.

MicroRNA-125b promotes neurons cell apoptosis and Tau phosphorylation in Alzheimer's disease.

Author information

1
Department of Geriatrics, Xi'an No. 1 Hospital, Xi'an 710002, China.
2
Open Ward, Qingdao Mental Health Center, Qingdao 266034, China.
3
Department of Geriatrics, Wuhan Mental Health Center, No. 93, Youyi Road, Qiaokou District, Wuhan 430022, China. Electronic address: mengjing0046@126.com.

Abstract

Alzheimer's disease (AD) is considered as one of the most common neural degenerative diseases in human. Although the continuous investigations about AD have been made in recent decades, the pathogenesis of this disease is still not definitely confirmed. MicroRNA-125b (miR-125b) is extensive expressed in many types of human tissues and played pivotal regulatory roles in diverse biological process. In the present study, we aimed to explore the roles of miR-125b in regulating neurons cell apoptosis under AD condition. The possible molecular mechanisms were also investigated. We found that miR-125b was up-regulated in patients with AD. Transfection with miR-125b significantly enhanced the apoptosis of neurons cells and phosphorylation of Tau by activation of cyclin-dependent kinase 5 (CDK5) and p35/25. Forkhead box Q1 (FOXQ1) was the direct target gene of miR-125b, which involved in the effects of miR-125b on neurons cell apoptosis and phosphorylation of Tau. Our research interpreted the mechanism of up-regulation of miR-125b in pathological Tau phosphorylation and AD occurrence. miR-125b may be a novel regulator of AD progress and could be as a therapeutic target for AD therapy.

KEYWORDS:

Alzheimer’s disease; Forkhead box Q1; MicroRNA-125b; Neurons cell apoptosis; Tau phosphorylation

PMID:
28947385
DOI:
10.1016/j.neulet.2017.09.043
[Indexed for MEDLINE]

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