ArticleTranslational research : the journal of laboratory and clinical medicine2018
Cilostazol, a phosphodiesterase 3 inhibitor, activates proteasome-mediated proteolysis and attenuates tauopathy and cognitive decline.
Article in Translational research : the journal of laboratory and clinical medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- Early proteasome downregulation and dysfunction drive proteostasis failure in Alzheimer's disease.Brain : a journal of neurology · 2025Article
- Comprehensive bioinformatic analysis identifies potential therapeutic drugs for CryAB (R120G)-related cardiomyopathy.BMC cardiovascular disorders · 2025Article
- Promoting proteostasis by cAMP/PKA and cGMP/PKG.Trends in molecular medicine · 2025Review
- The ubiquitin-proteasome system in Alzheimer's disease: mechanism of action and current status of treatment.Frontiers in aging neuroscience · 2025Review
- Understanding neurodevelopmental proteasomopathies as new rare disease entities: A review of current concepts, molecular biomarkers, and perspectives.Genes & diseases · 2024Review
- Cytosolic DNA initiates a vicious circle of aging-related endothelial inflammation and mitochondrial dysfunction via STING: the inhibitory effect of Cilostazol.Acta pharmacologica Sinica · 2024Article
- Proteotoxic stress and the ubiquitin proteasome system.Seminars in cell & developmental biology · 2024Review
- Emerging Potential of the Phosphodiesterase (PDE) Inhibitor Ibudilast for Neurodegenerative Diseases: An Update on Preclinical and Clinical Evidence.Molecules (Basel, Switzerland) · 2022Review
- Phosphodiesterase (PDE) III inhibitor, Cilostazol, improved memory impairment in aluminum chloride-treated rats: modulation of cAMP/CREB pathway.Inflammopharmacology · 2022Article
- Roflumilast Reduces Pathological Symptoms of Sporadic Alzheimer's Disease in Rats Produced by Intracerebroventricular Streptozotocin by Inhibiting NF-κB/BACE-1 Mediated Aβ Production in the Hippocampus and Activating the cAMP/BDNF Signalling Pathway.Neurotoxicity research · 2022Article
- [Neuroprotective treatment of tauopathies].Der Nervenarzt · 2021Review
- Advances in Proteasome Enhancement by Small Molecules.Biomolecules · 2021Review
- P62 accumulates through neuroanatomical circuits in response to tauopathy propagation.Acta neuropathologica communications · 2021Article
- PAC1 receptor-mediated clearance of tau in postsynaptic compartments attenuates tau pathology in mouse brain.Science translational medicine · 2021Article
- Mechanisms That Activate 26S Proteasomes and Enhance Protein Degradation.Biomolecules · 2021Review
- Priming the Proteasome to Protect against Proteotoxicity.Trends in molecular medicine · 2020Review
- cGMP via PKG activates 26S proteasomes and enhances degradation of proteins, including ones that cause neurodegenerative diseases.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Alzheimer Cells on Their Way to Derailment Show Selective Changes in Protein Quality Control Network.Frontiers in molecular biosciences · 2020Article
- Pharmacological Potential of Cilostazol for Alzheimer's Disease.Frontiers in pharmacology · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease and several variants of frontotemporal degeneration including progressive supranuclear palsy and corticobasal degeneration are characterized by the accumulation of abnormal tau protein into aggregates. Most proteins, including tau, are degraded via the ubiquitin proteasome system, but when abnormal tau accumulates, the function of 26S proteasomes is downregulated. The negative effect of tau aggregates on the function of the proteasome can have deleterious consequences on protein homeostasis and disease progression. Developing therapies aimed at clearing abnormal tau are thus of considerable interest. In the present study, we investigated the effect of cilostazol, an FDA-approved selective phosphodiesterase 3 inhibitor, on a mouse model of tauopathy (line rTg4510). Administration of cilostazol for 30 days enhanced proteasome function via the cyclic adenosine 3',5'-monophosphate/protein kinase A pathway and attenuated tauopathy and cognitive decline in rTg4510 mice. These results suggest that cilostazol, or other FDA-approved drugs acting via the same pathway, has the potential to be repurposed for the treatment of patients with early-stage tauopathy.
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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.