Mechanisms Underlying Dysregulation of miR-132 in Alzheimer's Disease.

• Type of Material: Article
• Authors: Qiaoyun Song, Emory University; Juan Dou, Emory University; Zixu Mao, Emory University; Zhexing Wen, Emory University; Wenming Li, Emory University
• Language: English
• Date: 2019
• Publisher: Biomedical
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © Wenming Li | Biomedical Journal of Science and Technical Research
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.26717/bjstr.2019.22.003824
• Title of Journal or Parent Work: Biomed J Sci Tech Res
• Volume: 22
• Issue: 5
• Start Page: 17018
• End Page: 17020
• Grant/Funding Information: The relevant work is partially supported by grants from NIH [AG058866 (WL), NS095269 and NS107505 (ZM)] and DoD [W81XWH1910353 (ZW)].
• Keywords: Alzheimer’s Disease; microRNAs

Abstract

Alzheimer’s disease (AD), the most common format of dementia, is an increasingly prevalent and complex neurogenerative disorder in the elderly and among the leading causes of a miserable life quality and death worldly and characterized pathologically by both abnormal plaques consisting of aggregated amyloid β (Aβ) and neurofibrillary tangles of hyperphosphorylated tau [1]. microRNAs (miRNAs), small non-coding RNAs that regulate the translation of targeted mRNAs, are predicted to regulate up to 90% of the genes in humans, suggesting that they may control every cellular process in all cells and tissues of the human body [2]. Not surprisingly, alterations of individual miRNAs have been implicated in the AD pathological condition. The number of miRNAs is dysregulated in the AD disease conditions. Several neuroprotective miRNAs, especially miR-132, are downregulated in the AD patient brain, while several neurodegenerative miRNAs are upregulated in the same AD context [3]. Identifying what reasons and mechanisms cause the differentiative expressions of miRNAs may be key to the understanding of AD pathogenesis and the approaching of miRNAs for the AD therapy. Here we take miR-132 as an example to briefly discuss what mechanisms mediate its dysregulation under Alzheimer’s conditions.