MicroRNA-195 downregulates Alzheimer's disease amyloid-β production by targeting BACE1
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease, characterized by amyloid-beta (Aβ) deposition and neurofibrillary tangles. Numerous microRNAs have been found to play crucial roles in regulating Aβ production in the process of AD. Previous investigations have reported lower levels of many microRNAs in AD patients and animal models. Here, we examined the role of miR-195 in the process of Aβ formation. Bioinformatics' algorithms predicted miR-195 binding sites within the beta-site APP cleaving enzyme 1 (BACE1) 3'-untranslated region (3'-UTR), and we found the level of miR-195 to be negatively related to the protein level of BACE1 in SAMP8 mice. We confirmed the target site in HEK293 cells by luciferase assay. Overexpression of miR-195 in N2a/WT cells decreased the BACE1 protein level, and inhibition of miR-195 resulted in increase of BACE1 protein level. Furthermore, overexpression of miR-195 in N2a/APP decreased the level of Aβ, while inhibition of miR-195 resulted in an increase of Aβ. Thus, we demonstrated that miR-195 could downregulate the level of Aβ by inhibiting the translation of BACE1. We conclude that miR-195 might provide a therapeutic strategy for AD.
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Several miRNAs have been identified as regulators of BACE1 expression.
“So far, several miRNAs have been identified as regulators of BACE1 expression (Hebert et al. 2008, Zong et al. 2011, Zhu et al. 2012, Fang et al. 2012, Wang et al. 2008b, Boissonneault et al. 2009, Long et al. 2014), suggesting that an extensive network of multiple miRNAs may regulate BACE1 expression in a coordinated manner.”
From miR‐186 is decreased in aged brain and suppresses <scp>BACE</scp>1 expression (2016) · cites this paper as Zhu et al. 2012
An extensive network of multiple miRNAs may regulate BACE1 expression in a coordinated manner.
“So far, several miRNAs have been identified as regulators of BACE1 expression (Hebert et al. 2008, Zong et al. 2011, Zhu et al. 2012, Fang et al. 2012, Wang et al. 2008b, Boissonneault et al. 2009, Long et al. 2014), suggesting that an extensive network of multiple miRNAs may regulate BACE1 expression in a coordinated manner.”
From miR‐186 is decreased in aged brain and suppresses <scp>BACE</scp>1 expression (2016) · cites this paper as Zhu et al. 2012
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References 38 · Cited by 204
- Authors
- Zhu, H.-C., Wang, L.-M., Wang, M., Song, B., Tan, S., Teng, J.-F., & Duan, D.-X.
- Affiliations
- First Affiliated Hospital of Zhengzhou University (CN)
- Zhengzhou University (CN)
- ORCID
- Venue
- Brain Research Bulletin
- Publisher
- Elsevier BV
- Published
- 2012-09
- Volume
- 88
- Issue
- 6
- Pages
- 596-601
- ISSN
- 0361-9230 (ISSN-L)
- OpenAlex
- W1991334828
- Cited by
- 204
- References
- 38
- Citations by year
- 2026: 5 · 2025: 14 · 2024: 11 · 2023: 18 · 2022: 18 · 2021: 19 · 2020: 19 · 2019: 23 · 2018: 17 · 2017: 9 · 2016: 12 · 2015: 12 · 2014: 10 · 2013: 15 · 2012: 2
- FWCI
- 8.37
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research Bulletin (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- miR-195, Alzheimer's disease, amyloid-beta production, BACE1, beta-site APP-cleaving enzyme 1, microRNA target regulation, 3' untranslated region, SAMP8 mice, APP overexpression, protein synthesis inhibition, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Binding Sites, Hippocampus, Humans, Mice, Neurologic Mutants, Neuroblastoma, Protein Processing, Post-Translational, Recombinant Fusion Proteins, RNA, Messenger, Protein Biosynthesis, Down-Regulation, Amyloid beta-Peptides, Aspartic Acid Endopeptidases, Mutagenesis, Site-Directed, Aging, Premature, 3' Untranslated Regions, RNA Stability, Protein Interaction Mapping, MicroRNAs, Cell Line, Tumor, Mice, Amyloid Precursor Protein Secretases, HEK293 Cells
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