ArticleThe Journal of clinical investigation2015
Dysregulation of microRNA-219 promotes neurodegeneration through post-transcriptional regulation of tau.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
113 citing papers in PubMed, 3 syntheses or guidelines pooled it, 204 citations in OpenAlex.
- Pooled it
- 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
- Interplay between brain-specific microRNAs and Alzheimer's disease.Neural regeneration research · 2026Article
- The Biological Basis, Mechanisms of Action, and Optimization Strategies of Exosomes Derived from Mesenchymal Stem Cells for the Treatment of Alzheimer's Disease.Molecular neurobiology · 2026Review
- PEARL: integrative multi-omics classification and omics feature discovery via deep graph learning.Bioinformatics (Oxford, England) · 2026Article
- The role of MicroRNAs in Alzheimer's disease: from pathogenesis to therapeutic potential.Molecular biology reports · 2026Review
- The Dual Role of the 16mer Motif Within the 3' Untranslated Region of the Variant Surface Glycoprotein of Trypanosoma brucei.Molecular microbiology · 2026Article
- Epigenetic Changes in Alzheimer's Disease and Interventions for Therapy.Neuropsychiatric disease and treatment · 2026Review
- MIRit: an integrative R framework for the identification of impaired miRNA-mRNA regulatory networks in complex diseases.Bioinformatics advances · 2026Article
- Review
- Regulation of miR-219 and its target RalGPS dictates acute synaptic plasticity at thebioRxiv : the preprint server for biology · 2025Article
- Prolonged Survival with Dieting for Improved Autophagy.Non-coding RNA · 2025Review
- MicroRNAs modulation by curcumin, catalpol, and other natural products in Alzheimer's disease: a review.Molecular biology reports · 2025Review
- Therapeutic potential and microRNA regulating properties of phytochemicals in Alzheimer's disease.Molecular therapy. Nucleic acids · 2025Review
- An Update on Neuroaging on Earth and in Spaceflight.International journal of molecular sciences · 2025Review
- Non-coding RNAs in the pathogenesis of Alzheimer's disease: β-amyloid aggregation, Tau phosphorylation and neuroinflammation.Molecular biology reports · 2025Review
- Hypermethylation and suppression of microRNA219a-2 activates the ALDH1L2/GSH/PAI-1 pathway for fibronectin degradation in renal fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Epigenetics Modulators as Therapeutics for Neurological Disorders.Current pharmaceutical design · 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
53 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Tau is a highly abundant and multifunctional brain protein that accumulates in neurofibrillary tangles (NFTs), most commonly in Alzheimer's disease (AD) and primary age-related tauopathy. Recently, microRNAs (miRNAs) have been linked to neurodegeneration; however, it is not clear whether miRNA dysregulation contributes to tau neurotoxicity. Here, we determined that the highly conserved brain miRNA miR-219 is downregulated in brain tissue taken at autopsy from patients with AD and from those with severe primary age-related tauopathy. In a Drosophila model that produces human tau, reduction of miR-219 exacerbated tau toxicity, while overexpression of miR-219 partially abrogated toxic effects. Moreover, we observed a bidirectional modulation of tau levels in the Drosophila model that was dependent on miR-219 expression or neutralization, demonstrating that miR-219 regulates tau in vivo. In mammalian cellular models, we found that miR-219 binds directly to the 3'-UTR of the tau mRNA and represses tau synthesis at the post-transcriptional level. Together, our data indicate that silencing of tau by miR-219 is an ancient regulatory mechanism that may become perturbed during neurofibrillary degeneration and suggest that this regulatory pathway may be useful for developing therapeutics for tauopathies.
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Registered trials
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.