ReviewBiomedicines2021
Critical Molecular and Cellular Contributors to Tau Pathology.
Review in Biomedicines, 2021. 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, 36 citations in OpenAlex.
- AHA1 Regulates Aβ Production via Modulation of APP Abundance and γ-Secretase Assembly.Journal of neurochemistry · 2026Article
- Zika virus infection induces a persistent accumulation of Alzheimer's disease-like Tau phosphorylation in adult immunocompetent mice in association with memory and social behavior impairments.Acta neuropathologica communications · 2026Article
- ThebioRxiv : the preprint server for biology · 2026Article
- The aging gut-glia-immune axis in alzheimer's disease: microbiome-derived mediators of neuroinflammation and therapeutic innovation.GeroScience · 2026Review
- The Potential Use of Matrix Metalloproteinases in Alzheimer's Disease Therapy.Journal of clinical medicine · 2026Review
- Twenty years of therapeutic development in tauopathy mouse models: a scoping review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The NLRP3-P2X7 Axis and Cytokine Crosstalk in Alzheimer's Disease: Mechanisms, Implications, and Therapeutic Opportunities.CNS & neurological disorders drug targets · 2025Review
- Designed Cell-Penetrating Peptide Constructs for Inhibition of Pathogenic Protein Self-Assembly.Pharmaceutics · 2024Review
- Cell-cell communication: new insights and clinical implications.Signal transduction and targeted therapy · 2024Review
- Neuroinflammation in Alzheimer's Disease: A Potential Role of Nose-Picking in Pathogen Entry via the Olfactory System?Biomolecules · 2023Review
- Emerging Roles of Cells and Molecules of Innate Immunity in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Role of Exosomes in the Pathogenesis and Theranostic of Alzheimer's Disease and Parkinson's Disease.International journal of molecular sciences · 2023Review
- Molecular Research on Alzheimer's Disease.Biomedicines · 2023Article
- The innate immune response in tauopathies.European journal of immunology · 2023Review
- Big Tau: What We Know, and We Need to Know.eNeuro · 2023Article
- Regulation of Tau Expression in Superior Cervical Ganglion (SCG) Neurons In Vivo and In Vitro.Cells · 2023Article
- Tau-dependent HDAC1 nuclear reduction is associated with altered VGluT1 expression.Frontiers in cell and developmental biology · 2023Article
- Microglia-Astrocyte Communication in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- The Interplay between GSK3β and Tau Ser262 Phosphorylation during the Progression of Tau Pathology.International journal of molecular sciences · 2022Article
- Heparan Sulfate Proteoglycans (HSPGs) Serve as the Mediator Between Monomeric Tau and Its Subsequent Intracellular ERK1/2 Pathway Activation.Journal of molecular neuroscience : MN · 2022Article
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
No grant is acknowledged in the PubMed record.
Abstract
Tauopathies represent a group of neurodegenerative diseases including Alzheimer's disease (AD) that are characterized by the deposition of filamentous tau aggregates in the brain. The pathogenesis of tauopathies starts from the formation of toxic 'tau seeds' from hyperphosphorylated tau monomers. The presence of specific phosphorylation sites and heat shock protein 90 facilitates soluble tau protein aggregation. Transcellular propagation of pathogenic tau into synaptically connected neuronal cells or adjacent glial cells via receptor-mediated endocytosis facilitate disease spread through the brain. While neuroprotective effects of glial cells-including phagocytotic microglial and astroglial phenotypes-have been observed at the early stage of neurodegeneration, dysfunctional neuronal-glial cellular communication results in a series of further pathological consequences as the disease progresses, including abnormal axonal transport, synaptic degeneration, and neuronal loss, accompanied by a pro-inflammatory microenvironment. Additionally, the discovery of microtubule-associated protein tau (
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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.