ArticleFrontiers in molecular neuroscience2011
Modulation of GSK-3 as a Therapeutic Strategy on Tau Pathologies.
Article in Frontiers in molecular neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 115 citations in OpenAlex.
- Valorization of 2-aminoethoxydiphenyl borate as a neurotherapeutic agent: modulation of calcineurin, TRPC1 and MARK2/GSK-3β signaling in scopolamine-triggered tauopathy.Inflammopharmacology · 2026Article
- Higher baseline CSF cortisol is associated with adverse 24-month tau-related, neuroimaging, and cognitive outcomes across the Alzheimer's disease continuum.European geriatric medicine · 2026Article
- Evaluation of the Nrf2-Keap1 Pathway in Patients with Acute Cerebral Ischemic Disease.Medicina (Kaunas, Lithuania) · 2026Article
- Neuroinflammation and Tauopathies.Molecular biology reports · 2026Review
- Protein Kinases in Alzheimer's Disease: Pioneering Insights into Pathogenesis and Therapeutic Breakthroughs.Current neuropharmacology · 2026Review
- Molecular interplay between glycogen synthase kinase 3 beta and A-kinase anchoring protein 11 in bipolar disorder: a narrative review.Frontiers in molecular neuroscience · 2026Review
- Mechanistic role of APOE lipidation in Alzheimer's disease pathogenesis.Theranostics · 2026Review
- Substance Abuse and Cognitive Decline: The Critical Role of Tau Protein as a Potential Biomarker.International journal of molecular sciences · 2025Review
- Liver function and Alzheimer's brain pathologies: A longitudinal study: Liver and Alzheimer's pathologies.The journal of prevention of Alzheimer's disease · 2025Article
- Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection.Molecular neurobiology · 2024Review
- Beyond Amyloid: A Machine Learning-Driven Approach Reveals Properties of Potent GSK-3β Inhibitors Targeting Neurofibrillary Tangles.International journal of molecular sciences · 2024Article
- Depressive-like Behaviors Induced by mGluR5 Reduction in 6xTg in Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Bilirubin and Redox Stress in Age-Related Brain Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Molecular docking, molecular dynamics simulations andRSC advances · 2023Article
- Combination of indirect revascularization and endothelial progenitor cell transplantation improved cerebral perfusion and ameliorated tauopathy in a rat model of bilateral ICA ligation.Stem cell research & therapy · 2022Article
- Marine Natural Products from the Russian Pacific as Sources of Drugs for Neurodegenerative Diseases.Marine drugs · 2022Review
- Rosiridin Attenuates Scopolamine-Induced Cognitive Impairments in Rats via Inhibition of Oxidative and Nitrative Stress Leaded Caspase-3/9 and TNF-α Signaling Pathways.Molecules (Basel, Switzerland) · 2022Article
- TDP-43 drives synaptic and cognitive deterioration following traumatic brain injury.Acta neuropathologica · 2022Article
- Benefits of dietary polyphenols in Alzheimer's disease.Frontiers in aging neuroscience · 2022Review
- Inhibition of Glycogen Synthase Kinase 3β Activity in the Basolateral Amygdala Disrupts Reconsolidation and Attenuates Heroin Relapse.Frontiers in molecular neuroscience · 2022Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycogen synthase kinase-3 (GSK-3) is ubiquitously expressed and unusually active in resting, non-stimulated cells. In mammals, at least three proteins (α, β1, and β2), generated from two different genes, gsk-3α and gsk-3β, are widely expressed at both the RNA and protein levels although some tissues show preferential expression of some of the three proteins. Control of GSK-3 activity occurs by complex mechanisms that depend on specific signaling pathways, often controlling the inhibition of the kinase activity. GSK-3 appears to integrate different signaling pathways from a wide selection of cellular stimuli. The unique position of GSK-3 in modulating the function of a diverse series of proteins and its association with a wide variety of human disorders has attracted significant attention as a therapeutic target and as a means to understand the molecular basis of brain disorders. Different neurodegenerative diseases including frontotemporal dementia, progressive supranuclear palsy, and Alzheimer's disease, present prominent tau pathology such as tau hyperphosphorylation and aggregation and are collectively referred to as tauopathies. GSK-3 has also been associated to different neuropsychiatric disorders, like schizophrenia and bipolar disorder. GSK-3β is the major kinase to phosphorylate tau both in vitro and in vivo and has been proposed as a target for therapeutic intervention. The first therapeutic strategy to modulate GSK-3 activity was the direct inhibition of its kinase activity. This review will focus on the signaling pathways involved in the control of GSK-3 activity and its pathological deregulation. We will highlight different alternatives of GSK-3 modulation including the direct pharmacological inhibition as compared to the modulation by upstream regulators.
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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.