ReviewAlzheimer's research & therapy2013
Potential synergy between tau aggregation inhibitors and tau chaperone modulators.
Review in Alzheimer's research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 28 citations in OpenAlex.
- Chaperone-Mediated Regulation of Tau Phase Separation, Fibrillation, and Toxicity.Journal of the American Chemical Society · 2025Article
- Mechanism of action deconvolution of the small-molecule pathological tau aggregation inhibitor Anle138b.Alzheimer's research & therapy · 2023Article
- FKBP51 modulates hippocampal size and function in post-translational regulation of Parkin.Cellular and molecular life sciences : CMLS · 2022Article
- Toxic Tau Oligomers Modulated by Novel Curcumin Derivatives.Scientific reports · 2019Article
- Article
- Brain proteomics links oxidative stress with metabolic and cellular stress response proteins in behavioural alteration of Alzheimer's disease model rats.AIMS neuroscience · 2019Article
- Therapeutic strategies and nano-drug delivery applications in management of ageing Alzheimer's disease.Drug delivery · 2018Review
- Hsp90 and FKBP51: complex regulators of psychiatric diseases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Review
- Therapeutic Strategies for Restoring Tau Homeostasis.Cold Spring Harbor perspectives in medicine · 2018Review
- Human iPSC-Derived Neuronal Model of Tau-A152T Frontotemporal Dementia Reveals Tau-Mediated Mechanisms of Neuronal Vulnerability.Stem cell reports · 2016Article
- Protein homeostasis gene dysregulation in pretangle-bearing nucleus basalis neurons during the progression of Alzheimer's disease.Neurobiology of aging · 2016Article
- Azaphilones inhibit tau aggregation and dissolve tau aggregates in vitro.ACS chemical neuroscience · 2015Article
- Synthesis, stereochemical analysis, and derivatization of myricanol provide new probes that promote autophagic tau clearance.ACS chemical biology · 2015Article
- Redox proteomics analysis to decipher the neurobiology of Alzheimer-like neurodegeneration: overlaps in Down's syndrome and Alzheimer's disease brain.The Biochemical journal · 2014Review
- Stages and conformations of the Tau repeat domain during aggregation and its effect on neuronal toxicity.The Journal of biological chemistry · 2014Article
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
Abstract
Tau is a soluble, microtubule-associated protein known to aberrantly form amyloid-positive aggregates. This pathology is characteristic for more than 15 neuropathies, the most common of which is Alzheimer's disease. Finding therapeutics to reverse or remove this non-native tau state is of great interest; however, at this time only one drug is entering phase III clinical trials for treating tauopathies. Generally, tau manipulation by therapeutics can either directly or indirectly alter tau aggregation and stability. Drugs that bind and change the conformation of tau itself are largely classified as aggregation inhibitors, while drugs that alter the activity of a tau-effector protein fall into several categories, such as kinase inhibitors, microtubule stabilizers, or chaperone modulators. Chaperone inhibitors that have proven effective in tau models include heat shock protein 90 inhibitors, heat shock protein 70 inhibitors and activators, as well as inducers of heat shock proteins. While many of these compounds can alter tau levels and/or aggregation states, it is possible that combining these approaches may produce the most optimal outcome. However, because many of these compounds have multiple off-target effects or poor blood-brain barrier permeability, the development of this synergistic therapeutic strategy presents significant challenges. This review will summarize many of the drugs that have been identified to alter tau biology, with special focus on therapeutics that prevent tau aggregation and regulate chaperone-mediated clearance of tau.
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.