ArticleMolecular therapy. Nucleic acids2020
miRNA-31 Improves Cognition and Abolishes Amyloid-β Pathology by Targeting APP and BACE1 in an Animal Model of Alzheimer's Disease.
Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 97 citations in OpenAlex.
- Treatment of animal models of Alzheimer's disease with extracellular vesicles or exosomes and involvement of microRNAs.Neural regeneration research · 2026Article
- ELAVL Proteins, miRNA Fate, and Extracellular RNA Communication in Brain Aging and Neurodegeneration.Cells · 2026Review
- Peripheral and Central miRNA Signatures in Alzheimer's Disease: Tissue-Specific Variability, Sex-Associated Differences, and Implications for Blood-Based Biomarkers.International journal of molecular sciences · 2026Review
- MicroRNAs in the pathogenesis of neurodegenerative disorders: Potential as therapeutic targets.Neural regeneration research · 2026Article
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- Development of a serum-based microRNA panel for Alzheimer's disease diagnosis.Journal of translational internal medicine · 2026Article
- Recent advances towards BACE1 drug discovery and therapeutics design.RSC medicinal chemistry · 2026Review
- Morpho-Functional Characterization and miRNA Profiling of the Retina in the 5xFAD Murine Model of Alzheimer's Disease.Investigative ophthalmology & visual science · 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
- miR-495-3p Attenuates Neuronal Apoptosis Through The Activation of Wnt/MAPK Pathways in Ischemic Stroke.Molecular neurobiology · 2025Article
- The neuroinflammatory role of microRNAs in Alzheimer's disease: pathological insights to therapeutic potential.Molecular and cellular biochemistry · 2025Review
- Longitudinal Evaluation of the Detection Potential of Serum Oligoelements Cu, Se and Zn for the Diagnosis of Alzheimer's Disease in the 3xTg-AD Animal Model.International journal of molecular sciences · 2025Article
- Physical exercise and epigenetic modifications in skeletal muscle, brain, and heart.Epigenetics & chromatin · 2025Review
- A review on gut microbiota and miRNA crosstalk: implications for Alzheimer's disease.GeroScience · 2025Review
- Polyphenols and miRNA interplay: a novel approach to combat apoptosis and inflammation in Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- In vivo and ex vivo gene therapy for neurodegenerative diseases: a promise for disease modification.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Nilotinib as a Prospective Treatment for Alzheimer's Disease: Effect on Proteins Involved in Neurodegeneration and Neuronal Homeostasis.Life (Basel, Switzerland) · 2024Article
- Insights into the Role of microRNAs as Clinical Tools for Diagnosis, Prognosis, and as Therapeutic Targets in Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Exploring the Regulatory Landscape of Dementia: Insights from Non-Coding RNAs.International journal of molecular sciences · 2024Review
- Downregulation of miR-181c-5p in Alzheimer's disease weakens the response of microglia to Aβ phagocytosis.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common form of dementia worldwide, characterized by progressive memory impairment, behavioral changes, and, ultimately, loss of consciousness and death. Recently, microRNA (miRNA) dysfunction has been associated with increased production and impaired clearance of amyloid-β (Aβ) peptides, whose accumulation is one of the most well-known pathophysiological markers of this disease. In this study, we identified several miRNAs capable of targeting key proteins of the amyloidogenic pathway. The expression of one of these miRNAs, miR-31, previously found to be decreased in AD patients, was able to simultaneously reduce the levels of APP and Bace1 mRNA in the hippocampus of 17-month-old AD triple-transgenic (3xTg-AD) female mice, leading to a significant improvement of memory deficits and a reduction in anxiety and cognitive inflexibility. In addition, lentiviral-mediated miR-31 expression significantly ameliorated AD neuropathology in this model, drastically reducing Aβ deposition in both the hippocampus and subiculum. Furthermore, the increase of miR-31 levels was enough to reduce the accumulation of glutamate vesicles in the hippocampus to levels found in non-transgenic age-matched animals. Overall, our results suggest that miR-31-mediated modulation of APP and BACE1 can become a therapeutic option in the treatment of AD.
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