MiR-124 acts as a target for Alzheimer’s disease by regulating BACE1

Abstract

// Fengmao An 1, 2, * , Guohua Gong 1, 2, 3, * , Yu Wang 1, 2 , Ming Bian 1, 2 , Lijun Yu 1, 2 and Chengxi Wei 1, 2 1 Medicinal Chemistry and Pharmacology Institute, Inner Mongolia University for The Nationalities, Tongliao, Inner Mongolia, P.R. China 2 Inner Mongolia Key Laboratory of Mongolian Medicine Pharmacology for Cardio-Cerebral Vascular System, Tongliao, Inner Mongolia, P.R. China 3 First Clinical Medical of Inner Mongolia University for Nationalities, Tongliao, Inner Mongolia, P.R. China * These authors have contributed equally to this work Correspondence to: Chengxi Wei, email: weichengxi1224@163.com Lijun Yu, email: tl_ylj@163.com Keywords: Alzheimer’s disease; miR-124; BACE1; cell viability; cell apoptosis Received: June 03, 2017 Accepted: November 03, 2017 Published: December 09, 2017 ABSTRACT Although large numbers of microRNAs (miRNAs) expressed in Alzheimer disease (AD) have been detected, their functions and mechanisms of regulation remain to be fully clarified. Beta-site Amyloid precursor protein Cleaving Enzyme 1 (BACE1) has been one of the prime therapeutic targets for AD. Here, we identified that miR-124 levels are gradually decreased in AD. In addition, we demonstrated that miR-124 suppresses BACE1 expression by directly targeting the 3′UTR of Bace1 mRNA in vitro . Inhibition of miR-124 significantly increased BACE1 levels in neuronal cells. In contrast, miR-124 overexpression significantly suppressed BACE1 expression in cells. And finally we determined that downregulation of miR-124 alleviated Aβ-induced viability inhibition and decreased apoptosis in SH-SY5Y cells. Our results demonstrated that miR-124 is a potent negative regulator of BACE1 in the cellular AD phenotype and might be involved in the pathogenesis of AD.

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