The selective GSK3 inhibitor, SAR502250, displays neuroprotective activity and attenuates behavioral impairments in models of neuropsychiatric symptoms of Alzheimer's disease in rodents
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Abstract Glycogen synthase kinase 3 (GSK3) has been identified as a promising target for the treatment of Alzheimer’s disease (AD), where abnormal activation of this enzyme has been associated with hyperphosphorylation of tau proteins. This study describes the effects of the selective GSK3 inhibitor, SAR502250, in models of neuroprotection and neuropsychiatric symptoms (NPS) associated with AD. In P301L human tau transgenic mice, SAR502250 attenuated tau hyperphosphorylation in the cortex and spinal cord. SAR502250 prevented the increase in neuronal cell death in rat embryonic hippocampal neurons following application of the neurotoxic peptide, Aβ25–35. In behavioral studies, SAR502250 improved the cognitive deficit in aged transgenic APP(SW)/Tau(VLW) mice or in adult mice after infusion of Aβ25–35. It attenuated aggression in the mouse defense test battery and improved depressive-like state of mice in the chronic mild stress procedure after 4 weeks of treatment. Moreover, SAR502250 decreased hyperactivity produced by psychostimulants. In contrast, the drug failed to modify anxiety-related behaviors or sensorimotor gating deficit. This profile confirms the neuroprotective effects of GSK3 inhibitors and suggests an additional potential in the treatment of some NPS associated with AD.
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GSK3 is a target for AD with promising results of the GSK3 inhibitor SAR502250 on neuroprotection and attenuation of behavioral alterations in AD mouse models.
“GSK3 is a target for AD with promising results of the GSK3 inhibitor SAR502250 on neuroprotection and attenuation of behavioral alterations in AD mouse models64.”
From Integrated analysis of behavioral, epigenetic, and gut microbiome analyses in AppNL-G-F, AppNL-F, and wild type mice (2021) · cites this paper as [64]
The Discussion reports that SAR502250 reduced tau hyperphosphorylation and neuronal cell death and improved some behaviors relevant to AD. However, the Discussion’s psychiatric-symptoms section says that, except for cognitive tasks, the behavioral results came from non-pathological models of AD; the claim overextends those results to AD mouse models generally. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIncreased GSK-3β activity induces Aβ deposition extracellularly.
“Furthermore, increased GSK-3β activity also induces Aβ deposition extracellularly (Griebel et al., 2019;Toral-Rios et al., 2020).”
From Multi-target neuroprotective effects of herbal medicines for Alzheimer's disease (2022) · cites this paper as Griebel et al., 2019
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Research works printed but not linked: 1
- [62]Griebel Guy Pichat Philippe Pruniaux Marie-Pierre Beeské Sandra Lopez-Grancha Mati Genet Elisabeth Terranova Jean-Paul Castro Antonio Sánchez Juan Antonio Black Mark Varty Geoffrey B. Weiner Ina Arad Michal Barak Segev De Levie Amaya Guillot Etienne SAR110894, a potent histamine H3-receptor antagonist, displays procognitive effects in rodents Pharmacology Biochemistry and Behavior 2012 102 2 203 214 10.1016/j.pbb.2012.04.004 22542742 · DOI
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- Authors
- Griebel, G., Stemmelin, J., Lopez-Grancha, M., Boulay, D., Boquet, G., Slowinski, F., Pichat, P., Beeské, S., Tanaka, S., Mori, A., Fujimura, M., & Eguchi, J.
- Affiliations
- Sanofi (France) (FR)
- Tanabe Pharma Corporation (Japan) (JP)
- Corresponding author
- Griebel, Guy
- Venue
- Scientific Reports
- Published
- 2019-12-02
- Volume
- 9
- Issue
- 1
- Pages
- 18045-18045
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC6888874
- OpenAlex
- W2991246038
- Cited by
- 97
- References
- 99
- Citations by year
- 2026: 5 · 2025: 15 · 2024: 12 · 2023: 16 · 2022: 19 · 2021: 16 · 2020: 14
- FWCI
- 8.40
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Pharmacology › Cholinesterase and Neurodegenerative Diseases
- Keywords
- GSK-3 inhibitors, Alzheimer's disease, neuropsychiatric symptoms, neuroprotection, tau hyperphosphorylation, amyloid beta 25-35, cognitive impairment, aggression, depression-like behavior, anxiety, sensorimotor gating
- MeSH terms
- Aggression, Alzheimer Disease, Animals, Behavior, Animal, Cells, Cultured, Cerebral Cortex, Disease Models, Animal, Drug Evaluation, Preclinical, Female, Humans, Male, Mice, Transgenic, Neurons, Phosphorylation, Spinal Cord, tau Proteins, Apoptosis, Neuroprotective Agents, Glycogen Synthase Kinase 3, Mice, Rats, Cognitive Dysfunction, Primary Cell Culture
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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