ArticlePloS one2015
GSK3β inhibition promotes synaptogenesis in Drosophila and mammalian neurons.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- USP11 drives stress-induced synaptic structural deficits and depression-like behaviors through GSK3β/mTOR signaling.Neurobiology of stress · 2026Article
- Alismatis Rhizoma prevents AβO-induced neuronal cell death and synaptic loss in Alzheimer's disease models.Frontiers in pharmacology · 2026Article
- From Better Diagnostics to Earlier Treatment: The Rapidly Evolving Alzheimer's Disease Landscape.Medicina (Kaunas, Lithuania) · 2025Review
- GSK3: A potential target and pending issues for treatment of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- Neurotrophic effects of intermittent fasting, calorie restriction and exercise: a review and annotated bibliography.Frontiers in aging · 2023Review
- Pridopidine Promotes Synaptogenesis and Reduces Spatial Memory Deficits in the Alzheimer's Disease APP/PS1 Mouse Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Alignment between glioblastoma internal clock and environmental cues ameliorates survival in Drosophila.Communications biology · 2022Article
- Glycogen synthase kinase-3 inhibition rescues sex-dependent contextual fear memory deficit in human immunodeficiency virus-1 transgenic mice.British journal of pharmacology · 2020Article
- Pharmacological Treatment of Alzheimer's Disease: Insights fromInternational journal of molecular sciences · 2020Review
- Frameshift mutations ofDisease models & mechanisms · 2020Article
- GSK3β: A Master Player in Depressive Disorder Pathogenesis and Treatment Responsiveness.Cells · 2020Review
- PI3K activation prevents Aβ42-induced synapse loss and favors insoluble amyloid deposit formation.Molecular biology of the cell · 2020Article
- Modulated Expression of the Protein Kinase GSK3 in Motor and Dopaminergic Neurons Increases Female Lifespan inFrontiers in genetics · 2020Article
- Disordered Expression ofInternational journal of molecular sciences · 2019Article
- Voltage-gated sodium currents in cerebellar Purkinje neurons: functional and molecular diversity.Cellular and molecular life sciences : CMLS · 2018Review
- Amyloid β42 peptide is toxic to non-neural cells inBiology open · 2017Article
- Neuronal NOS Induces Neuronal Differentiation Through a PKCα-Dependent GSK3β Inactivation Pathway in Hippocampal Neural Progenitor Cells.Molecular neurobiology · 2017Article
- The equilibrium between antagonistic signaling pathways determines the number of synapses in Drosophila.PloS one · 2017Article
- Isoflurane Is More Deleterious to Developing Brain Than Desflurane: The Role of the Akt/GSK3β Signaling Pathway.BioMed research international · 2016Article
- The PI3K signaling pathway as a pharmacological target in Autism related disorders and Schizophrenia.Molecular and cellular therapies · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The PI3K-dependent activation of AKT results in the inhibition of GSK3β in most signaling pathways. These kinases regulate multiple neuronal processes including the control of synapse number as shown for Drosophila and rodents. Alzheimer disease's patients exhibit high levels of circulating GSK3β and, consequently, pharmacological strategies based on GSK3β antagonists have been designed. The approach, however, has yielded inconclusive results so far. Here, we carried out a comparative study in Drosophila and rats addressing the role of GSK3β in synaptogenesis. In flies, the genetic inhibition of the shaggy-encoded GSK3β increases the number of synapses, while its upregulation leads to synapse loss. Likewise, in three weeks cultured rat hippocampal neurons, the pharmacological inhibition of GSK3β increases synapse density and Synapsin expression. However, experiments on younger cultures (12 days) yielded an opposite effect, a reduction of synapse density. This unexpected finding seems to unveil an age- and dosage-dependent differential response of mammalian neurons to the stimulation/inhibition of GSK3β, a feature that must be considered in the context of human adult neurogenesis and pharmacological treatments for Alzheimer's disease based on GSK3β antagonists.
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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.