ArticleFrontiers in molecular neuroscience2011
GSK3 and Alzheimer's Disease: Facts and Fiction….
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 82 papers, 1 of them a synthesis that pooled it.
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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
82 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.
- Cognitive Decline in Preclinical Alzheimer's Disease: Amyloid-Beta versus Tauopathy.Journal of Alzheimer's disease : JAD · 2018Pooled it
- Effect of PHF-1 hyperphosphorylation on the seeding activity of C-terminal Tau fragments.Scientific reports · 2025Article
- Danggui Shaoyao San Alleviates Early Cognitive Impairment in Alzheimer's Disease Mice Through IRS1/GSK3β/Wnt3a-β-Catenin Pathway.Brain and behavior · 2024Article
- Ellagic acid improves the symptoms of early-onset Alzheimer's disease: Behavioral and physiological correlates.Heliyon · 2024Article
- A scoping review of mathematical models covering Alzheimer's disease progression.Frontiers in neuroinformatics · 2024Article
- Loss of calcium/calmodulin-dependent protein kinase kinase 2, transferrin, and transferrin receptor proteins in the temporal cortex of Alzheimer's patients postmortem is associated with abnormal iron homeostasis: implications for patient survival.Frontiers in cell and developmental biology · 2024Article
- Depressive-like Behaviors Induced by mGluR5 Reduction in 6xTg in Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2023Article
- The Multifaceted Role of WNT Signaling in Alzheimer's Disease Onset and Age-Related Progression.Cells · 2023Review
- Targeting CaN/NFAT in Alzheimer's brain degeneration.Frontiers in immunology · 2023Review
- APPsα rescues CDK5 and GSK3β dysregulation and restores normal spine density in Tau transgenic mice.Frontiers in cellular neuroscience · 2023Article
- The Identification of Blood Biomarkers of Chronic Neuropathic Pain by Comparative Transcriptomics.Neuromolecular medicine · 2022Article
- In Silico Molecular Docking Analysis of Karanjin against Alzheimer's and Parkinson's Diseases as a Potential Natural Lead Molecule for New Drug Design, Development and Therapy.Molecules (Basel, Switzerland) · 2022Article
- Glycogen Synthase Kinase 3: Ion Channels, Plasticity, and Diseases.International journal of molecular sciences · 2022Review
- Molecular Insights to the Wnt Signaling During Alzheimer's Disorder: a Potential Target for Therapeutic Interventions.Journal of molecular neuroscience : MN · 2022Review
- Meridianins Rescue Cognitive Deficits, Spine Density and Neuroinflammation in the 5xFAD Model of Alzheimer's Disease.Frontiers in pharmacology · 2022Article
- Lithium modulates multiple tau kinases with distinct effects in cortical and hippocampal neurons according to concentration ranges.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Glycogen Synthase Kinase 3β: A New Gold Rush in Anti-Alzheimer's Disease Multitarget Drug Discovery?Journal of medicinal chemistry · 2021Article
- The GSK-3 Inhibitor CT99021 Enhances the Acquisition of Spatial Learning and the Accuracy of Spatial Memory.Frontiers in molecular neuroscience · 2021Article
- Alzheimer's Disease and Protein Kinases.Advances in experimental medicine and biology · 2021Article
- CAMKK2-CAMK4 signaling regulates transferrin trafficking, turnover, and iron homeostasis.Cell communication and signaling : CCS · 2020Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The physiological functions and pathological roles of the Glycogen synthase kinase-type 3 (GSK3) kinases in peripheral and central systems are diverse and complex, and therefore hard to unravel in molecular detail in vivo. Our assignment to review and discuss available data to clarify the actual position of these kinases in the pathology of Alzheimer's dementia (AD) was both ambitious and easy. On the one hand, numerous studies are available in isolated, recombinant, or cell-based systems, which have resulted in very diverse data-sets that are hardly informative for the brain in vivo. At the other extreme, reliable, and relevant models for the role of GSK3 in CNS are rare, if not lacking. Moreover, (too) many in vivo studies used Li(+) as "specific" inhibitor of GSK3, which is factually not valid because lithium ions are neither specific nor potent inhibitors of GSK3 in vivo. More specific pharmacological inhibitors of GSK3 have met with considerable problems, and are reviewed by others in this issue or elsewhere. We concentrate here on AD-related aspects of GSK3 in brain in vivo, mainly studied in transgenic mice and highlight some of the more important issues, among many remaining: activation of GSK3 by amyloid, phosphorylation of protein tau, effects on or interference with synaptic activity, differentiation between both GSK3 isoforms. These relate directly to brain function, and brain dysfunction in AD, and are to be resolved if we want to understand the molecular pathology of this dreadful disease.
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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.