ReviewCold Spring Harbor perspectives in medicine2018
Therapeutic Strategies for Restoring Tau Homeostasis.
Review in Cold Spring Harbor perspectives in medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- A metabolite extracted from Escherichia coli suppresses tau aggregation.The Biochemical journal · 2026Article
- Synthetic chaperone based on Hsp90-Tau interaction inhibits Tau aggregation and rescues physiological Tau-Microtubule interaction.Nature communications · 2025Article
- Phosphorylation of tau at a single residue inhibits binding to the E3 ubiquitin ligase, CHIP.Nature communications · 2024Article
- Selenoprotein W modulates tau homeostasis in an Alzheimer's disease mouse model.Communications biology · 2024Article
- Article
- Activation of transient receptor potential vanilloid 1 ameliorates tau accumulation-induced synaptic damage and cognitive dysfunction via autophagy enhancement.CNS neuroscience & therapeutics · 2024Article
- Disease-Modifying Therapies for Alzheimer's Disease: More Questions than Answers.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Small heat shock protein 22 kDa can modulate the aggregation and liquid-liquid phase separation behavior of tau.Protein science : a publication of the Protein Society · 2021Article
- Inhibitors of heat shock protein 70 (Hsp70) with enhanced metabolic stability reduce tau levels.Bioorganic & medicinal chemistry letters · 2021Article
- Combating deleterious phase transitions in neurodegenerative disease.Biochimica et biophysica acta. Molecular cell research · 2021Review
- Prion-Like Propagation Mechanisms in Tauopathies and Traumatic Brain Injury: Challenges and Prospects.Biomolecules · 2020Review
- Management of Hsp90-Dependent Protein Folding by Small Molecules Targeting the Aha1 Co-Chaperone.Cell chemical biology · 2020Article
- Tau Post-translational Modifications: Dynamic Transformers of Tau Function, Degradation, and Aggregation.Frontiers in neurology · 2020Review
- Molecular Chaperones: A Double-Edged Sword in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2020Review
- Compromised function of the ESCRT pathway promotes endolysosomal escape of tau seeds and propagation of tau aggregation.The Journal of biological chemistry · 2019Article
- Modulation of Amyloid States by Molecular Chaperones.Cold Spring Harbor perspectives in biology · 2019Review
- Mapping interactions with the chaperone network reveals factors that protect against tau aggregation.Nature structural & molecular biology · 2018Article
- Our Working Point of View of Tau Protein.Journal of Alzheimer's disease : JAD · 2018Review
- An inhibitor of the proteasomal deubiquitinating enzyme USP14 induces tau elimination in cultured neurons.The Journal of biological chemistry · 2017Article
- Cognitive Decline in Neuronal Aging and Alzheimer's Disease: Role of NMDA Receptors and Associated Proteins.Frontiers in neuroscience · 2017Review
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
Normal tau homeostasis is achieved when the synthesis, processing, and degradation of the protein is balanced. Together, the pathways that regulate tau homeostasis ensure that the protein is at the proper levels and that its posttranslational modifications and subcellular localization are appropriately controlled. These pathways include the enzymes responsible for posttranslational modifications, those systems that regulate mRNA splicing, and the molecular chaperones that control tau turnover and its binding to microtubules. In tauopathies, this delicate balance is disturbed. Tau becomes abnormally modified by posttranslational modification, it loses affinity for microtubules, and it accumulates in proteotoxic aggregates. How and why does this imbalance occur? In this review, we discuss how molecular chaperones and other components of the protein homeostasis (e.g., proteostasis) network normally govern tau quality control. We also discuss how aging might reduce the capacity of these systems and how tau mutations might further affect this balance. Finally, we discuss how small-molecule inhibitors are being used to probe and perturb the tau quality-control systems, playing a particularly prominent role in revealing the logic of tau homeostasis. As such, there is now interest in developing these chemical probes into therapeutics, with the goal of restoring normal tau homeostasis to treat disease.
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.