ArticleInternational journal of Alzheimer's disease2012
MicroRNAs and the Regulation of Tau Metabolism.
Article in International journal of Alzheimer's disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Pooled it
- RNA-based therapeutics for Alzheimer's disease and related tauopathies: challenges and opportunities.The journal of prevention of Alzheimer's disease · 2026Review
- Circular RNAs, miRNAs, and Exosomes: Their Roles and Importance in Amyloid-Beta and Tau Pathologies in Alzheimer's Disease.Neural plasticity · 2025Review
- Pathophysiological Aspects and Therapeutic Armamentarium of Alzheimer's Disease: Recent Trends and Future Development.Cellular and molecular neurobiology · 2023Review
- Posttranscriptional regulation of neurofilament proteins and tau in health and disease.Brain research bulletin · 2023Review
- Role of miRNAs in Neurodegeneration: From Disease Cause to Tools of Biomarker Discovery and Therapeutics.Genes · 2022Review
- Cognitive dysfunction associated with COVID-19: Prognostic role of circulating biomarkers and microRNAs.Frontiers in aging neuroscience · 2022Review
- miRNAs as Therapeutic Tools in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Regional and temporal miRNAs expression profile in a transgenic mouse model of tauopathy: implication for its pathogenesis.Molecular psychiatry · 2021Article
- MicroRNA-298 reduces levels of human amyloid-β precursor protein (APP), β-site APP-converting enzyme 1 (BACE1) and specific tau protein moieties.Molecular psychiatry · 2021Article
- Integrated miRNA-Seq and mRNA-Seq Study to Identify miRNAs Associated With Alzheimer's Disease Using Post-mortem Brain Tissue Samples.Frontiers in neuroscience · 2021Article
- Advances and Challenges in Understanding MicroRNA Function in Tauopathies: A Case Study of miR-132/212.Frontiers in neurology · 2020Article
- Presymptomatic change in microRNAs modulates Tau pathology.Scientific reports · 2018Article
- Differential expression of microRNAs and other small RNAs in muscle tissue of patients with ALS and healthy age-matched controls.Scientific reports · 2018Article
- MicroRNA-322 Cluster Promotes Tau Phosphorylation via Targeting Brain-Derived Neurotrophic Factor.Neurochemical research · 2018Article
- MicroRNAs in glaucoma and neurodegenerative diseases.Journal of human genetics · 2017Review
- The miR-132/212 locus: a complex regulator of neuronal plasticity, gene expression and cognition.RNA & disease (Houston, Tex.) · 2016Article
- Frontotemporal Lobar Degeneration and MicroRNAs.Frontiers in aging neuroscience · 2016Review
- Opposite effects of two estrogen receptors on tau phosphorylation through disparate effects on the miR-218/PTPA pathway.Aging cell · 2015Article
- The epigenetics of aging and neurodegeneration.Progress in neurobiology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal regulation of tau phosphorylation and/or alternative splicing is associated with the development of a large (>20) group of neurodegenerative disorders collectively known as tauopathies, the most common being Alzheimer's disease. Despite intensive research, little is known about the molecular mechanisms that participate in the transcriptional and posttranscriptional regulation of endogenous tau, especially in neurons. Recently, we showed that mice lacking Dicer in the forebrain displayed progressive neurodegeneration accompanied by disease-like changes in tau phosphorylation and splicing. Dicer is a key enzyme in the biogenesis of microRNAs (miRNAs), small noncoding RNAs that function as part of the RNA-induced silencing complex (RISC) to repress gene expression at the posttranscriptional level. We identified miR-16 and miR-132 as putative endogenous modulators of neuronal tau phosphorylation and tau exon 10 splicing, respectively. Interestingly, these miRNAs have been implicated in cell survival and function, whereas changes in miR-16/132 levels correlate with tau pathology in human neurodegenerative disorders. Thus, understanding how miRNA networks influence tau metabolism and possibly other biological systems might provide important clues into the molecular causes of tauopathies, particularly the more common but less understood sporadic forms.
Identifiers
What OpenQuestion holds
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.