ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
MiR-26b, upregulated in Alzheimer's disease, activates cell cycle entry, tau-phosphorylation, and apoptosis in postmitotic neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 2 of them syntheses that pooled it.
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Who cites it
157 citing papers in PubMed, 2 syntheses or guidelines pooled it, 288 citations in OpenAlex.
- A Systematic Review of MicroRNA Expression as Biomarker of Late-Onset Alzheimer's Disease.Molecular neurobiology · 2019Pooled it
- Systematic Review of miRNA as Biomarkers in Alzheimer's Disease.Molecular neurobiology · 2019Pooled it
- Deregulation of Synaptic Plasticity-Related MicroRNAs After Repetitive Transcranial Magnetic Stimulation in Alzheimer's Disease.Molecular neurobiology · 2026Trial
- Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer's disease.Ageing research reviews · 2026Review
- MicroRNAs in the pathogenesis of neurodegenerative disorders: Potential as therapeutic targets.Neural regeneration research · 2026Article
- Interplay between brain-specific microRNAs and Alzheimer's disease.Neural regeneration research · 2026Article
- Review
- Plasma miRNAs associated with cognitive impairment and brain hypometabolism in individuals with mild cognitive impairment.BMC neurology · 2026Article
- Morpho-Functional Characterization and miRNA Profiling of the Retina in the 5xFAD Murine Model of Alzheimer's Disease.Investigative ophthalmology & visual science · 2026Article
- Differentially expressed miRNAs in the temporal cortex of Alzheimer's disease patients and their association to tau pathology.Communications biology · 2026Article
- Epigenetics in Alzheimer's disease: from molecular mechanisms to emerging novel biomarkers.Frontiers in aging neuroscience · 2026Review
- Article
- An overview of gene and cell therapy approaches for Alzheimer's disease.Metabolic brain disease · 2025Review
- MicroRNAs in neurodegenerative diseases: from molecular mechanisms to clinical biomarkers, detection methods and therapeutic strategies-advances and challenges.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Melatonin Supplementation in Alzheimer's disease: The Potential Role in Neurogenesis.Molecular neurobiology · 2025Review
- Circulating Biomarkers for the Early Diagnosis of Alzheimer's Disease.International journal of molecular sciences · 2025Review
- miRNAs in neurodegenerative diseases: from target screening to precision therapy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025Article
- Non-coding RNAs in the pathogenesis of Alzheimer's disease: β-amyloid aggregation, Tau phosphorylation and neuroinflammation.Molecular biology reports · 2025Review
- c-Triadem: A constrained, explainable deep learning model to identify novel biomarkers in Alzheimer's disease.PloS one · 2025Article
97 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
MicroRNA (miRNA) functions in the pathogenesis of major neurodegenerative diseases such as Alzheimer's disease (AD) are only beginning to emerge. We have observed significantly elevated levels of a specific miRNA, miR-26b, in the defined pathological areas of human postmortem brains, starting from early stages of AD (Braak III). Ectopic overexpression of miR-26b in rat primary postmitotic neurons led to the DNA replication and aberrant cell cycle entry (CCE) and, in parallel, increased tau-phosphorylation, which culminated in the apoptotic cell death of neurons. Similar tau hyperphosphorylation and CCE are typical features of neurons in pre-AD brains. Sequence-specific inhibition of miR-26b in culture is neuroprotective against oxidative stress. Retinoblastoma protein (Rb1), a major tumor suppressor, appears as the key direct miR-26b target, which mediates the observed neuronal phenotypes. The downstream signaling involves upregulation of Rb1/E2F cell cycle and pro-apoptotic transcriptional targets, including cyclin E1, and corresponding downregulation of cell cycle inhibitor p27/Kip1. It further leads to nuclear export and activation of Cdk5, a major kinase implicated in tau phosphorylation, regulation of cell cycle, and death in postmitotic neurons. Therefore, upregulation of miR-26b in neurons causes pleiotropic phenotypes that are also observed in AD. Elevated levels of miR-26b may thus contribute to the AD neuronal pathology.
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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.