ReviewInternational journal of molecular sciences2022
Phosphorylated Tau in Alzheimer's Disease and Other Tauopathies.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 270 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
270 citing papers in PubMed, 1 synthesis or guideline pooled it, 391 citations in OpenAlex.
- Genetic correlates of corticobasal degeneration: a systematic review and meta-analysis.Journal of neurology · 2026Pooled it
- Article
- STZ‑induced sporadic Alzheimer's in rats: behavioral, histopathological, and MiRNA profiles.Journal of molecular histology · 2026Article
- Article
- Oxidative stress and inflammation in neurodegenerative disorders.Archives of toxicology · 2026Review
- Functional and structural characterization of dendritic spine pathology in a mouse model of tauopathy.iScience · 2026Article
- Temporal Trajectories of the Tau Aggregate Interactome Reveal Stage-Specific Vulnerabilities in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transcriptomic Signatures of Microglial Phagocytosis Reveal Diagnostic Markers and Immune Landscape in Alzheimer's Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Virobiome-mediated regulation of microbiota-gut-brain axis signaling and neuroimmune homeostasis.Cell communication and signaling : CCS · 2026Review
- Emerging diagnostic biomarkers and therapeutic targets in Alzheimer's disease.Inflammopharmacology · 2026Review
- When copper turns killer: Decoding copper dyshomeostasis and cuproptosis in neurodegenerative pathogenesis and precision metal interventions.Neural regeneration research · 2026Article
- Plasma Concentrations of Amyloid-β Peptides, BACE-1, and Tau Proteins in Alzheimer's Disease.Turkish journal of pharmaceutical sciences · 2026Article
- Review
- The Machine Learning Classification of Retinal Ganglion Cell Dendritic Texture in a 3xTg-Alzheimer's Disease Mouse Model.Diagnostics (Basel, Switzerland) · 2026Article
- Multi-omics profiling reveals gut microbiome signatures associated with cognitive decline in Alzheimer's disease.iScience · 2026Article
- Protease-Mediated TAR DNA-Binding Protein 43 (TDP-43) Pathogenesis: From Molecular Mechanisms to Therapeutic Opportunities.ACS pharmacology & translational science · 2026Review
- Tau dysfunction in alzheimer's disease: molecular and cellular mechanisms, genetic modulation, and therapeutic perspectives.Molecular biology reports · 2026Review
- Epitranscriptomic imprints on glial cell polarization: METTL3/IGF2BP2 axis as a driver of neurodegeneration in Alzheimer's disease.Psychopharmacology · 2026Review
- Genetic frontotemporal degeneration across the lifespan? A critical appraisal of the neurodevelopmental hypothesis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Tau physiology and pathology: impacts on cellular structures and neurodegenerative diseases.Inflammopharmacology · 2026Review
210 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
6 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the leading cause of dementia in elderly people. Amyloid beta (Aβ) deposits and neurofibrillary tangles are the major pathological features in an Alzheimer's brain. These proteins are highly expressed in nerve cells and found in most tissues. Tau primarily provides stabilization to microtubules in the part of axons and dendrites. However, tau in a pathological state becomes hyperphosphorylated, causing tau dysfunction and leading to synaptic impairment and degeneration of neurons. This article presents a summary of the role of tau, phosphorylated tau (p-tau) in AD, and other tauopathies. Tauopathies, including Pick's disease, frontotemporal dementia, corticobasal degeneration, Alzheimer's disease, argyrophilic grain disease, progressive supranuclear palsy, and Huntington's disease, are the result of misprocessing and accumulation of tau within the neuronal and glial cells. This article also focuses on current research on the post-translational modifications and genetics of tau, tau pathology, the role of tau in tauopathies and the development of new drugs targeting p-tau, and the therapeutics for treating and possibly preventing 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.