ReviewJournal of Alzheimer's disease : JAD2018
Modeling Prion-Like Processing of Tau Protein in Alzheimer's Disease for Pharmaceutical Development.
Review in Journal of Alzheimer's disease : JAD, 2018. 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
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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.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Concentration-Dependent Activity of Hydromethylthionine on Cognitive Decline and Brain Atrophy in Mild to Moderate Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Trial
- Potential of Low Dose Leuco-Methylthioninium Bis(Hydromethanesulphonate) (LMTM) Monotherapy for Treatment of Mild Alzheimer's Disease: Cohort Analysis as Modified Primary Outcome in a Phase III Clinical Trial.Journal of Alzheimer's disease : JAD · 2018Trial
- Quantification of plasma tau species containing the proline-rich region as a biomarker in Alzheimer's disease.Scientific reports · 2025Article
- Hydromethylthionine sustains truncated tau-dependent inflammation-lowering effects in mouse brain.The FEBS journal · 2025Article
- Vulnerability of the entorhinal cortex II to neurodegeneration in Alzheimer's disease.Brain communications · 2025Article
- Decoding Neurodegeneration: A Review of Molecular Mechanisms and Therapeutic Advances in Alzheimer's, Parkinson's, and ALS.International journal of molecular sciences · 2024Review
- High-affinity antibodies specific to the core region of the tau protein exhibit diagnostic and therapeutic potential for Alzheimer's disease.Alzheimer's research & therapy · 2024Article
- Very low levels of ABCA7 in the cerebrum and Alzheimer's disease onset between the ages of 60 and 80 independently of APOE.Journal of neuropathology and experimental neurology · 2024Article
- Mechanism of Methylene Blue Inducing the Disulfide Bond Formation of Tubulin-Associated Unit Proteins.JACS Au · 2024Article
- Considerations for biomarker strategies in clinical trials investigating tau-targeting therapeutics for Alzheimer's disease.Translational neurodegeneration · 2024Review
- Assays for the Screening and Characterization of Tau Aggregation Inhibitors.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Polymerization of recombinant tau core fragmentsFrontiers in neuroscience · 2023Article
- Reassessment of Neuronal Tau Distribution in Adult Human Brain and Implications for Tau Pathobiology.Acta neuropathologica communications · 2022Article
- HMTM-Mediated Enhancement of Brain Bioenergetics in a Mouse Tauopathy Model Is Blocked by Chronic Administration of Rivastigmine.Biomedicines · 2022Article
- The propagation mechanisms of extracellular tau in Alzheimer's disease.Journal of neurology · 2022Review
- Perivascular spaces as a potential biomarker of Alzheimer's disease.Frontiers in neuroscience · 2022Review
- Article
- Molecular Processing of Tau Protein in Progressive Supranuclear Palsy: Neuronal and Glial Degeneration.Journal of Alzheimer's disease : JAD · 2021Article
- Dephosphorylation Passivates the Seeding Activity of Oligomeric Tau Derived From Alzheimer's Brain.Frontiers in molecular neuroscience · 2021Article
- Tau in Alzheimer's Disease: Pathological Alterations and an Attractive Therapeutic Target.Current medical science · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following our discovery of a fragment from the repeat domain of tau protein as a structural constituent of the PHF-core in Alzheimer's disease (AD), we developed an assay that captured several key features of the aggregation process. Tau-tau binding through the core tau fragment could be blocked by the same diaminophenothiazines found to dissolve proteolytically stable PHFs isolated from AD brain. We found that the PHF-core tau fragment is inherently capable of auto-catalytic self-propagation in vitro, or "prion-like processing", that has now been demonstrated for several neurodegenerative disorders. Here we review the findings that led to the first clinical trials to test tau aggregation inhibitor therapy in AD as a way to block this cascade. Although further trials are still needed, the results to date suggest that a treatment targeting the prion-like processing of tau protein may have a role in both prevention and treatment of AD.
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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.