ReviewMolecular neurobiology2022
Tau Toxicity in Neurodegeneration.
Review in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Research trends and hotspots for frontotemporal dementia from 2000 to 2022: a bibliometric analysis.Frontiers in neurology · 2024Pooled it
- Assessment of Efficacy and Safety of Zagotenemab: Results From PERISCOPE-ALZ, a Phase 2 Study in Early Symptomatic Alzheimer Disease.Neurology · 2024Trial
- Article
- Autophagy and selective autophagy receptors: Key players against Alzheimer's disease.Neural regeneration research · 2026Article
- Prospect in Alzheimer's disease integrative therapy targeting both amyloid-beta and tau.Neural regeneration research · 2026Article
- Repeated mild spinal cord contusions exacerbate tauopathy development in PS19 mice.Acta neuropathologica communications · 2026Article
- Circular RNA circTrpc6-induced tau phosphorylation contributes to neuronal injury and cognitive decline via miR-485-5p/eIF4E axis in senescence-accelerated mouse prone 8 mice.Cell biology and toxicology · 2026Article
- FTDP-17T Mutations Promote Formation of Phosphorylated FTDP-17T TAU Oligomers That Cause Degeneration of Dopaminergic and Hippocampal Neurons via Activating ER Stress and Mitochondrial Pro-apoptotic Cascades.Neurochemical research · 2026Article
- Article
- Examining of the mechanism by which Yin Huang Ge compound alleviates cognitive dysfunction in Alzheimer's disease mice through modulation of Aβ degrading enzymes and neurotrophic factors.Frontiers in aging neuroscience · 2026Article
- (Alkyl-ω-ol)triphenyltin(IV)-Loaded Mesoporous Silica as Biocompatible Potential Neuroprotectors: Evaluation of Inhibitory Activity Against Enzymes Associated with the Pathophysiology of Alzheimer's Disease.Nanomaterials (Basel, Switzerland) · 2025Article
- Morphological and Molecular Profiling of Amyloid-β Species in Alzheimer's Pathogenesis.Molecular neurobiology · 2025Review
- Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances.Signal transduction and targeted therapy · 2025Review
- The Link Between Matrix Metalloproteinases and Alzheimer's Disease Pathophysiology.Molecular neurobiology · 2025Review
- Unveiling Role of Gut Microbiota in Alzheimer's Disease: Mechanisms, Challenges and Future Perspectives.Current Alzheimer research · 2025Review
- Bee Pollen as a Source of Biopharmaceuticals for Neurodegeneration and Cancer Research: A Scoping Review and Translational Prospects.Molecules (Basel, Switzerland) · 2024Article
- Epigenetic Mechanisms of Aluminum-Induced Neurotoxicity and Alzheimer's Disease: A Focus on Non-Coding RNAs.Neurochemical research · 2024Review
- Rottlerin Enhances the Autophagic Degradation of Phosphorylated Tau in Neuronal Cells.Molecular neurobiology · 2024Article
- Tau in neurodegenerative diseases: molecular mechanisms, biomarkers, and therapeutic strategies.Translational neurodegeneration · 2024Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Tau is a microtubule-associated protein widely distributed in the central nervous system (CNS). The main function of tau is to promote the assembly of microtubules and stabilize their structure. After a long period of research on neurodegenerative diseases, the function and dysfunction of the microtubule-associated protein tau in neurodegenerative diseases and tau neurotoxicity have attracted increasing attention. Tauopathies are a series of progressive neurodegenerative diseases caused by pathological changes in tau, such as abnormal phosphorylation. The pathological features of tauopathies are the deposition of abnormally phosphorylated tau proteins and the aggregation of tau proteins in neurons. This article first describes the normal physiological function and dysfunction of tau proteins and then discusses the enzymes and proteins involved in tau phosphorylation and dephosphorylation, the role of tau in cell dysfunction, and the relationships between tau and several neurodegenerative diseases. The study of tau neurotoxicity provides new directions for the treatment of tauopathies.
Indexed as
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.