MiR-361-3p inhibits β-amyloid accumulation and attenuates cognitive deficits through targeting BACE1 in Alzheimer's disease

• Main Author: Yangfei Ji, Dan Wang, Boai Zhang, Hong Lu
• Format: Article
• Language: English
• Published: IMR (Innovative Medical Research) Press Limited 2019-09-01
• Series: Journal of Integrative Neuroscience
• Subjects: |alzheimer’s disease|mir-361-3p|bace1|app-β|cognitive deficits|appswe cell
• Online Access: https://jin.imrpress.com/fileup/1757-448X/PDF/1569287160791-1027641834.pdf

The role of miR-361-3p in the pathology of Alzheimer’s disease is unknown. The target scan was used to screen potential target genes of miR-361-3p, and β-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) was emphasized. Results from western blotting and reverse transcription-quantitative polymerase chain reaction (RT-PCR) showed that down-regulated miR-361-3p was correlated with up-regulated BACE1 in Alzheimer’s disease patients’ brains. Luciferase assay confirmed that miR-361-3p directly targets BACE1. MiR-361-3p overexpression and knockdown experiments were performed and found that miR-361-3p could regulate the expression of BACE1, and the accumulation of APP-β in APPswe transfected SH-SY5Y cell. A Morris water maze test was performed and showed that overexpression of miR-361-3p improved cognitive deficits in APP/PS1 mice. We found miR-361-3p inhibited β-amyloid accumulation by targeting BACE1, which thus weakened cognitive deficits in Alzheimer's disease.