ReviewBiochimica et biophysica acta. Molecular cell research2020
Glycogen synthase kinase-3 signaling in Alzheimer's disease.
Review in Biochimica et biophysica acta. Molecular cell research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 317 papers, 6 of them syntheses that pooled it.
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
317 citing papers in PubMed, 6 syntheses or guidelines pooled it, 567 citations in OpenAlex.
- Extracellular Vesicle-Derived microRNAs as Fluid Biomarkers in Neurodegenerative Diseases: A Systematic Review.Journal of neurochemistry · 2026Pooled it
- Evidence of the Efficacy of Acetylcholinesterase Inhibitors inCNS & neurological disorders drug targets · 2026Pooled it
- The Role of c-Abl in Alzheimer's Disease: Guilty or not Guilty?Cellular and molecular neurobiology · 2025Pooled it
- Systematic Review on Neurotoxic Implications of Lead-Induced Gene Expression Alterations in the Etiology of Alzheimer's Disease.Cellular and molecular neurobiology · 2025Pooled it
- Meta-Analysis of Transcriptomic Studies of Blood and Six Brain Regions Identifies a Consensus of 15 Cross-Tissue Mechanisms in Alzheimer's Disease and Suggests an Origin of Cross-Study Heterogeneity.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2025Pooled it
- Efficacy and Safety of Natural Apigenin Treatment for Alzheimer's Disease: Focus onCurrent neuropharmacology · 2025Pooled it
- Integrative Transcriptomic and Interactome Analyses Prioritize Candidate Genes for Alzheimer's Disease.Molecular neurobiology · 2026Article
- Current Landscape of Glycogen Synthase Kinase-3β PET Tracers: Progress, Limitations, and Perspectives-A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Hyperglycemia associated brain dysfunction: rodent models for studying diabetic cognitive deficits.Metabolic brain disease · 2026Review
- PLCG2 downregulation impairs synaptic function and increases Alzheimer's disease hallmarks in neuronal cultures.Nature genetics · 2026Article
- Review
- The beneficial properties of CBDA in diet-induced neuroinflammation.Inflammopharmacology · 2026Article
- Article
- Blood metal signatures and their association with Alzheimer's disease risk and cognitive decline in an Egyptian cohort.Communications medicine · 2026Article
- Clinical Significance and Changes in Levels of Serum BDNF, mBDNF, AQP4, proBDNF, and GSK3β in Individuals Diagnosed With Bipolar Disorder: A Cross-Sectional Study.Health science reports · 2026Article
- Increased p-Tau181 Levels After Overnight Wakefulness Are Associated With Neuroticism in Young Women.Journal of sleep research · 2026Article
- MINERVA: a public XAI-powered platform advancing multi-target discovery in Alzheimer's disease.Journal of cheminformatics · 2026Article
- Role Shift of Glial Cells from Physiology to Pathology in Alzheimer's Disease: The Regulatory Impact of Exercise.Neuroscience bulletin · 2026Review
- Targeting the crosstalk between Alzheimer's disease and gastrointestinal cancers.Molecular medicine (Cambridge, Mass.) · 2026Review
- Article
257 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most common form of neurodegenerative disorder with dementia, accounting for approximately 70% of the all cases. Currently, 5.8 million people in the U.S. are living with AD and by 2050 this number is expected to double resulting in a significant socio-economic burden. Despite intensive research, the exact mechanisms that trigger AD are still not known and at the present there is no cure for it. In recent years, many signaling pathways associated with AD neuropathology have been explored as possible candidate targets for the treatment of this condition including glycogen synthase kinase-3β (GSK3-β). GSK3-β is considered a key player in AD pathophysiology since dysregulation of this kinase influences all the major hallmarks of the disease including: tau phosphorylation, amyloid-β production, memory, neurogenesis and synaptic function. The present review summarizes the current understanding of the GSK3-β neurobiology with particular emphasis on its effects on specific signaling pathways associated with AD pathophysiology. Moreover, it discusses the feasibility of targeting GSK3-β for AD treatment and provides a summary of the current research effort to develop GSK3-β inhibitors in preclinical and clinical studies.
Indexed as
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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.