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Genetics and Molecular Biology

Print version ISSN 1415-4757On-line version ISSN 1678-4685

Abstract

DU, Wenyan; LEI, Chengbin  and  DONG, Yong. MicroRNA-149 is downregulated in Alzheimer’s disease and inhibits β-amyloid accumulation and ameliorates neuronal viability through targeting BACE1. Genet. Mol. Biol. [online]. 2021, vol.44, n.1, e20200064.  Epub Jan 11, 2021. ISSN 1678-4685.  http://dx.doi.org/10.1590/1678-4685-gmb-2020-0064.

Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) plays a critical role in Alzheimer’s disease (AD) pathogenesis. This study aimed to investigate the relationship between microRNA-149 (miR-149) and BACE1, and evaluate the clinical significance and biological function of miR-149 in AD progression. Bioinformatics analysis and a luciferase reporter assay were used to confirm the interaction between miR-149 and BACE1. Expression of miR-149 and BACE1 was estimated using quantitative real-time PCR. The clinical significance of miR-149 in AD diagnosis and severity determination was evaluated using ROC analysis. The effect of miR-149 on Aβ accumulation and neuronal viability was analyzed in Aβ-treated SH-SY5Y cells. miR-149 was found directly binding the 3’-UTR of BACE1 and was negatively correlated with BACE1 in AD patients and cell model. Serum miR-149 expression was downregulated in AD patients and served as a potential diagnostic biomarker. The overexpression of miR-149 in Aβ-treated SH-SY5Y cells resulted in inhibited Aβ accumulation and enhanced neuronal viability. This study demonstrated that serum miR-149 is decreased in AD patients and serves as a candidate diagnostic biomarker, and that the overexpression of miR-149 may suppress Aβ accumulation and promote neuronal viability by targeting BACE1 in AD model cells.

Keywords : MicroRNA-149; Alzheimer’s disease; BACE1; diagnosis; APP.

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