ArticleJournal of neurochemistry2016
miR-186 is decreased in aged brain and suppresses BACE1 expression.
Article in Journal of neurochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- Non-coding RNAs involved in the molecular pathology of Alzheimer's disease: a systematic review.Frontiers in neuroscience · 2024Pooled it
- Exercise - induced changes in cerebrospinal fluid miRNAs in Gulf War Illness, Chronic Fatigue Syndrome and sedentary control subjects.Scientific reports · 2017Trial
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- MicroRNAs and Long Non-Coding RNAs Affect the Mechanisms Involved in Age-Related Neurodegeneration in a Manner Depending on RNA-Binding Proteins.Molecular neurobiology · 2026Review
- Mental health and gut-brain crosstalk: implications for depression and Alzheimer's disease.Neuroscience applied · 2026Review
- Early detection of Alzheimer's disease using small RNAs. Results from the EPAD cohort.The journal of prevention of Alzheimer's disease · 2025Article
- Dysregulated microRNAs in blood correlate with central nervous system neuropathology of prion disease.Veterinary research · 2025Article
- Non-coding RNAs in the pathogenesis of Alzheimer's disease: β-amyloid aggregation, Tau phosphorylation and neuroinflammation.Molecular biology reports · 2025Review
- Direct and indirect role of non-coding RNAs in company with amyloid and tau protein in promoting neuroinflammation in post-ischemic brain neurodegeneration.Frontiers in cellular neuroscience · 2025Review
- The Role of Non-Coding RNAs in Mitochondrial Dysfunction of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2024Review
- miR-NPs-RVG promote spinal cord injury repair: implications from spinal cord-derived microvascular endothelial cells.Journal of nanobiotechnology · 2024Article
- MicroRNAs: pioneering regulators in Alzheimer's disease pathogenesis, diagnosis, and therapy.Translational psychiatry · 2024Review
- Alzheimer's Disease-Related Epigenetic Changes: Novel Therapeutic Targets.Molecular neurobiology · 2024Review
- Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.Physiological reviews · 2024Review
- miR-3940-5p reduces amyloid β production via selectively targetingFrontiers in aging neuroscience · 2024Article
- MicroRNA biomarkers as next-generation diagnostic tools for neurodegenerative diseases: a comprehensive review.Frontiers in molecular neuroscience · 2024Review
- Potential Implications of miRNAs in the Pathogenesis, Diagnosis, and Therapeutics of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Specific downregulation of microRNA-186 induces neural stem cell self-renewal by upregulating Bmi-1/FoxG1 expression.Human cell · 2023Article
- Discerning the Prospects of miRNAs as a Multi-Target Therapeutic and Diagnostic for Alzheimer's Disease.Molecular neurobiology · 2023Review
- Roles of Non-Coding RNA in Alzheimer's Disease Pathophysiology.International journal of molecular sciences · 2023Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Accumulation of amyloid β (Aβ) in the brain is a key pathological hallmark of Alzheimer's disease (AD). Because aging is the most prominent risk factor for AD, understanding the molecular changes during aging is likely to provide critical insights into AD pathogenesis. However, studies on the role of miRNAs in aging and AD pathogenesis have only recently been initiated. Identifying miRNAs dysregulated by the aging process in the brain may lead to novel understanding of molecular mechanisms of AD pathogenesis. Here, we identified that miR-186 levels are gradually decreased in cortices of mouse brains during aging. In addition, we demonstrated that miR-186 suppresses β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) expression by directly targeting the 3'UTR of Bace1 mRNA in neuronal cells. In contrast, inhibition of endogenous miR-186 significantly increased BACE1 levels in neuronal cells. Importantly, miR-186 over-expression significantly decreased Aβ level by suppressing BACE1 expression in cells expressing human pathogenic mutant amyloid precursor protein. Taken together, our data demonstrate that miR-186 is a potent negative regulator of BACE1 in neuronal cells and it may be one of the molecular links between brain aging and the increased risk for AD during aging. We identified that miR-186 levels are gradually decreased in mouse cortices during aging. Furthermore, we demonstrated that miR-186 is a novel negative regulator of beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1) expression in neuronal cells. Therefore, we proposed that reduction in miR-186 levels during aging may lead to the up-regulation of BACE1 in the brain, thereby increasing a risk for Alzheimer's disease in aged individuals. Read the Editorial Highlight for this article on page 308.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.