ReviewBiochemical Society transactions2012
Brain-penetrant microtubule-stabilizing compounds as potential therapeutic agents for tauopathies.
Review in Biochemical Society transactions, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 42 citations in OpenAlex.
- Review
- Home-administered unfocused transcranial ultrasound in subjective cognitive decline and dementia: an open-label, uncontrolled feasibility pilot study.Frontiers in aging neuroscience · 2026Article
- Microtubule-Targeting Agents: Advances in Tubulin Binding and Small Molecule Therapy for Gliomas and Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Article
- Preliminary mechanistic insights of a brain-penetrant microtubule imaging PET ligand in a tau-knockout mouse model.EJNMMI research · 2022Article
- Crosstalk between acetylation and the tyrosination/detyrosination cycle of α-tubulin in Alzheimer's disease.Frontiers in cell and developmental biology · 2022Article
- Review
- Efficacy of epothilones in central nervous system trauma treatment: what has age got to do with it?Neural regeneration research · 2021Article
- Postnatal Role of the Cytoskeleton in Adult Epileptogenesis.Cerebral cortex communications · 2020Article
- Microtubules: A Key to Understand and Correct Neuronal Defects in CDKL5 Deficiency Disorder?International journal of molecular sciences · 2019Review
- Neuroprotective Approach of Anti-Cancer Microtubule Stabilizers Against Tauopathy Associated Dementia: Current Status of Clinical and Preclinical Findings.Journal of Alzheimer's disease reports · 2019Review
- Interaction between a MAPT variant causing frontotemporal dementia and mutant APP affects axonal transport.Neurobiology of aging · 2018Article
- Microfluidic platforms for the study of neuronal injury in vitro.Biotechnology and bioengineering · 2018Review
- The Microtubule-Modulating Drug Epothilone D Alters Dendritic Spine Morphology in a Mouse Model of Mild Traumatic Brain Injury.Frontiers in cellular neuroscience · 2018Article
- Evaluation of the brain-penetrant microtubule-stabilizing agent, dictyostatin, in the PS19 tau transgenic mouse model of tauopathy.Acta neuropathologica communications · 2016Article
- Combination of PKCε Activation and PTP1B Inhibition Effectively Suppresses Aβ-Induced GSK-3β Activation and Tau Phosphorylation.Molecular neurobiology · 2016Article
- MicroRNA-146a suppresses ROCK1 allowing hyperphosphorylation of tau in Alzheimer's disease.Scientific reports · 2016Article
- Characterization of Brain-Penetrant Pyrimidine-Containing Molecules with Differential Microtubule-Stabilizing Activities Developed as Potential Therapeutic Agents for Alzheimer's Disease and Related Tauopathies.The Journal of pharmacology and experimental therapeutics · 2016Article
- Salidroside reduces tau hyperphosphorylation via up-regulating GSK-3β phosphorylation in a tau transgenicTranslational neurodegeneration · 2016Article
- A Review of Systemic Treatment in Metastatic Triple-Negative Breast Cancer.Breast cancer : basic and clinical research · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Neurons within the brains of those with AD (Alzheimer's disease) and related neurodegenerative disorders, collectively termed 'tauopathies', contain fibrillar inclusions composed of hyperphosphorylated tau protein. Tau is normally enriched in axons, where it binds and stabilizes MTs (microtubules). Tau hyperphosphorylation and aggregation probably result in reduced MT binding that could affect axonal transport and neuronal function. A possible therapeutic strategy to overcome a loss of tau function in tauopathies is administration of MT-stabilizing agents, such as those used in the treatment of cancer. However, these drugs elicit severe side effects, and most existing MT-stabilizing compounds have poor BBB (blood-brain barrier) permeability, which renders them unsuitable for tauopathy treatment. We identified EpoD (epothilone D) as a brain-penetrant MT-stabilizing agent with preferred pharmacokinetic and pharmacodynamic properties. EpoD was evaluated for its ability to compensate for tau loss-of-function in an established Tg (transgenic) mouse model, using both preventative and interventional dosing paradigms. EpoD at doses much lower than previously used in human cancer patients caused improved axonal MT density and decreased axonal dystrophy in the tau Tg mice, leading to an alleviation of cognitive deficits. Moreover, EpoD reduced the extent of tau pathology in aged tau Tg mice. Importantly, no adverse side effects were observed in the EpoD-treated mice. These results suggest that EpoD might be a viable drug candidate for the treatment of AD and related tauopathies.
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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.