ReviewPharmacology & therapeutics2012
Tau as a therapeutic target in neurodegenerative disease.
Review in Pharmacology & therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 112 citations in OpenAlex.
- Article
- Neuronal Calcium Signaling and Cytoskeletal Dynamics in Neurodegeneration.International journal of molecular sciences · 2026Review
- The Application of Polymeric Nanoparticles as Drug Delivery Carriers to Cells in Neurodegenerative Diseases.Cell proliferation · 2025Review
- Association of the digital clock drawing test with amyloid and tau PET biomarkers in low age risk adults.Scientific reports · 2025Article
- Natural products against tau hyperphosphorylation-induced aggregates: Potential therapies for Alzheimer's disease.Archiv der Pharmazie · 2025Review
- Nanotechnology for tau pathology in Alzheimer's disease.Materials today. Bio · 2024Review
- Liquid-liquid phase separation in Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2024Review
- The Role of Inositol Hexakisphosphate Kinase in the Central Nervous System.Biomolecules · 2023Review
- Levosimendan inhibits disulfide tau oligomerization and ameliorates tau pathology in TauExperimental & molecular medicine · 2023Article
- Aggregation of Disordered Proteins Associated with Neurodegeneration.International journal of molecular sciences · 2023Review
- Tau Toxicity in Neurodegeneration.Molecular neurobiology · 2022Review
- Manipulation of the diet-microbiota-brain axis in Alzheimer's disease.Frontiers in neuroscience · 2022Review
- α-Synuclein Induces the GSK-3-Mediated Phosphorylation and Degradation of NURR1 and Loss of Dopaminergic Hallmarks.Molecular neurobiology · 2021Article
- The Structure Biology of Tau and Clue for Aggregation Inhibitor Design.The protein journal · 2021Review
- Recent advances in cellular biosensor technology to investigate tau oligomerization.Bioengineering & translational medicine · 2021Review
- Is PROTAC technology really a game changer for central nervous system drug discovery?Expert opinion on drug discovery · 2021Article
- When Good Kinases Go Rogue: GSK3, p38 MAPK and CDKs as Therapeutic Targets for Alzheimer's and Huntington's Disease.International journal of molecular sciences · 2021Review
- From Hybrids to New Scaffolds: The Latest Medicinal Chemistry Goals in Multi-target Directed Ligands for Alzheimer's Disease.Current neuropharmacology · 2021Review
- Use of Biodegradable, Chitosan-Based Nanoparticles in the Treatment of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2020Review
- Therapeutic Trem2 activation ameliorates amyloid-beta deposition and improves cognition in the 5XFAD model of amyloid deposition.Journal of neuroinflammation · 2020Article
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 1 institution in 1 country.
Funding
Abstract
Tau is a microtubule-associated protein thought to help modulate the stability of neuronal microtubules. In tauopathies, including Alzheimer's disease and several frontotemporal dementias, tau is abnormally modified and misfolded resulting in its disassociation from microtubules and the generation of pathological lesions characteristic for each disease. A recent surge in the population of people with neurodegenerative tauopathies has highlighted the immense need for disease-modifying therapies for these conditions, and new attention has focused on tau as a potential target for intervention. In the current work we summarize evidence linking tau to disease pathogenesis and review recent therapeutic approaches aimed at ameliorating tau dysfunction. The primary therapeutic tactics considered include kinase inhibitors and phosphatase activators, immunotherapies, small molecule inhibitors of protein aggregation, and microtubule-stabilizing agents. Although the evidence for tau-based treatments is encouraging, additional work is undoubtedly needed to optimize each treatment strategy for the successful development of safe and effective therapeutics.
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.