ReviewAnnual review of medicine2023
All the Tau We Cannot See.
Review in Annual review of medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 31 citations in OpenAlex.
- Prospect in Alzheimer's disease integrative therapy targeting both amyloid-beta and tau.Neural regeneration research · 2026Article
- Amyloid-β PET Radioligands in Alzheimer's Disease: From Plaque Detection to Biomarker-Guided Patient Stratification and Therapeutic Monitoring.Molecular diagnosis & therapy · 2026Review
- Cofactor-Free Tau Filaments Are Dynamic and Undergo Structural Evolution Driven by Thermodynamic Control.Journal of the American Chemical Society · 2026Article
- Elimination of tau tangles and soluble aggregates with the small molecule ACI-16664 prevents neurodegeneration in vivo.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Tau368 improves p-tau diagnostic accuracy for FTLD-tau from FTLD-TDP.Acta neuropathologica · 2026Article
- Alzheimer's disease: from molecular pathways to therapies.Molecular biomedicine · 2026Review
- Targeting tau in Alzheimer's Disease: rationale, approach and challenges.Molecular neurodegeneration · 2026Review
- Age-dependent vulnerability to spatial memory interference in APP/PS1 mice.Frontiers in aging neuroscience · 2026Article
- 4R-tau seeding activity reveals molecular subtypes in progressive supranuclear palsy.Nature communications · 2025Article
- Aberrant S293 Phosphorylation Drives Oligomerization of Tau Repeat R2: Insights from Molecular Dynamics Simulations.ACS chemical neuroscience · 2025Article
- Structural exposure of different microtubule binding domains determines the propagation and toxicity of pathogenic tau conformers in Alzheimer's disease.PLoS pathogens · 2025Article
- Polyoxometalates bind multiple targets involved in Alzheimer's disease.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2025Article
- Aggregate-selective removal of pathological tau by clustering-activated degraders.Science (New York, N.Y.) · 2024Article
- Rapidly reversible persistent long-term potentiation inhibition by patient-derived brain tau and amyloid ß proteins.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Article
- Advanced computational approaches to understand protein aggregation.Biophysics reviews · 2024Review
- The Enigma of Tau Protein Aggregation: Mechanistic Insights and Future Challenges.International journal of molecular sciences · 2024Review
- Phenotype parallels protein seeding capacity in neurodegenerative diseases.Brain pathology (Zurich, Switzerland) · 2024Article
- The role of the Pin1-Frontiers in cell and developmental biology · 2024Review
- Toward an animal model of Progressive Supranuclear Palsy.Frontiers in neuroscience · 2024Review
- Quantitative Measurement of Tau Aggregation in Genetically Modified Rats with Neurodegeneration.Methods in molecular biology (Clifton, N.J.) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) was described in 1906 as a dementing disease marked by the presence of two types of fibrillar aggregates in the brain: neurofibrillary tangles and senile plaques. The process of aggregation and formation of the aggregates has been a major focus of investigation ever since the discoveries that the tau protein is the predominant protein in tangles and amyloid β is the predominant protein in plaques. The idea that smaller, oligomeric species of amyloid may also be bioactive has now been clearly established. This review examines the possibility that soluble, nonfibrillar, bioactive forms of tau-the "tau we cannot see"-comprise a dominant driver of neurodegeneration in AD.
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.