IMR Press / JIN / Volume 18 / Issue 3 / DOI: 10.31083/j.jin.2019.03.1136
Open Access Original Research
MiR-361-3p inhibits β-amyloid accumulation and attenuates cognitive deficits through targeting BACE1 in Alzheimer's disease
Show Less
1 Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan Province, 450001, P. R. China
2 Department of Cardiology, Zhengzhou Central Hospital, Zhengzhou City, Henan Province, 450001, P. R. China
*Correspondence: (Hong Lu)
J. Integr. Neurosci. 2019, 18(3), 285–291;
Submitted: 20 April 2019 | Accepted: 31 July 2019 | Published: 30 September 2019
Copyright: © 2019 The authors. Published by IMR press.
This is an open access article under the CC BY-NC 4.0 license (

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.

Alzheimer’s disease
cognitive deficits
APPswe cell
Figure 1.
Back to top