ReviewNeurobiology of disease2020
Tau-mediated dysregulation of RNA: Evidence for a common molecular mechanism of toxicity in frontotemporal dementia and other tauopathies.
Review in Neurobiology of disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
25 citing papers in PubMed, 40 citations in OpenAlex.
- Review
- Riboregulation: a non-canonical tau function.Molecular neurodegeneration · 2026Review
- Meta-cancer phosphoproteomic analysis unveils association of Tau phosphosites with DNA damage response.Frontiers in systems biology · 2026Article
- Unraveling the molecular mechanisms in severe Alzheimer's disease based on transcriptomic data using next generation knowledge discovery methods.Pakistan journal of medical sciences · 2026Article
- Recent molecular insights and biosensor-based diagnostic technologies for hyperphosphorylated Tau in Alzheimer's disease.Alzheimer's research & therapy · 2025Review
- Article
- Making tau amyloid models in vitro: a crucial and underestimated challenge.FEBS letters · 2025Review
- Insights into pathophysiology, biomarkers, and therapeutics in tauopathies: Proceedings of the Tau2024 Global Conference.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau.Nature communications · 2025Article
- Pathogenic oligomeric Tau alters neuronal RNA processes through the formation of nuclear heteromeric amyloids with RNA-binding protein Musashi1.Progress in neurobiology · 2025Article
- TDP-43-proteinopathy at the crossroads of tauopathy: on copathology and current and prospective biomarkers.Frontiers in cellular neuroscience · 2025Review
- Decoding TDP-43: the molecular chameleon of neurodegenerative diseases.Acta neuropathologica communications · 2024Review
- m6A-dependent circular RNA formation mediates tau-induced neurotoxicity.bioRxiv : the preprint server for biology · 2024Article
- ZCCHC17 Modulates Neuronal RNA Splicing and Supports Cognitive Resilience in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Aging, NRF2, and TAU: A Perfect Match for Neurodegeneration?Antioxidants (Basel, Switzerland) · 2023Review
- Investigation of early molecular alterations in tauopathy with generative adversarial networks.Scientific reports · 2023Article
- CRISPRi screening reveals regulators of tau pathology shared between exosomal and vesicle-free tau.Life science alliance · 2023Article
- Tau Isoforms: Gaining Insight intoInternational journal of molecular sciences · 2022Review
- New Statement about NRF2 in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.Biomolecules · 2022Article
- The Role of TDP-43 in Neurodegenerative Disease.Molecular neurobiology · 2022Review
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 1 institution in 1 country.
Funding
Abstract
Frontotemporal dementias (FTDs) encompass several disorders commonly characterized by progressive frontotemporal lobar degeneration and dementia. Pathologically, TDP-43, FUS, dipeptide repeats, and tau constitute the protein aggregates in FTD, which in turn coincide with heterogeneity in clinical variants. The underlying molecular etiology explaining the formation of each type of protein aggregate remains unclear; however, dysregulated RNA metabolism rises as a common pathogenic factor. Alongside with TDP-43 and FUS, which bind to and regulate RNA dynamics, emerging data suggest that tau may also regulate RNA metabolism and translation. The complex mechanisms that drive translational selectivity in turn regulate the broad clinical presentation of FTDs. Here, we focus on the enigmatic relationship between tau and RNA and review the mechanisms of tau-mediated dysregulation of RNA in tauopathies such as FTD.
Indexed as
Identifiers
What Socratic 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 Socratic graph.