A novel GSK-3β inhibitor reduces Alzheimer's pathology and rescues neuronal loss in vivo
Open accessAbstract
Amyloid deposits, neurofibrillary tangles, and neuronal cell death in selectively vulnerable brain regions are the chief hallmarks in Alzheimer's (AD) brains. Glycogen synthase kinase-3 (GSK-3) is one of the key kinases required for AD-type abnormal hyperphosphorylation of tau, which is believed to be a critical event in neurofibrillary tangle formation. GSK-3 has also been recently implicated in amyloid precursor protein (APP) processing/Abeta production, apoptotic cell death, and learning and memory. Thus, GSK-3 inhibition represents a very attractive drug target in AD and other neurodegenerative disorders. To investigate whether GSK-3 inhibition can reduce amyloid and tau pathologies, neuronal cell death and memory deficits in vivo, double transgenic mice coexpressing human mutant APP and tau were treated with a novel non-ATP competitive GSK-3beta inhibitor, NP12. Treatment with this thiadiazolidinone compound resulted in lower levels of tau phosphorylation, decreased amyloid deposition and plaque-associated astrocytic proliferation, protection of neurons in the entorhinal cortex and CA1 hippocampal subfield against cell death, and prevention of memory deficits in this transgenic mouse model. These results show that this novel GSK-3 inhibitor has a dual impact on amyloid and tau alterations and, perhaps even more important, on neuronal survival in vivo further suggesting that GSK-3 is a relevant therapeutic target in AD.
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Tideglusib has been reported to reduce tau phosphorylation and has anti-inflammatory effects in animal models.
“Tideglusib has been reported to reduce tau phosphorylation and has anti-inflammatory effects in animal models [216, 217].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [216]
Tideglusib in preclinical double transgenic mice expressing human tau and APP reduced tau phosphorylation, decreased amyloid deposition, led to less neuronal loss, and improved cognition.
“A GSK-3 inhibitor, tideglusib, was shown in a preclinical study using double transgenic mice expressing human tau and APP to reduce tau phosphorylation, decrease amyloid deposition, lead to less neuronal loss and improved cognition (Serenó et al., 2009).”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Serenó et al., 2009
In animal models of AD, tideglusib reduces tau phosphorylation, Aβ plaque burden, memory deficits, cell death and astrocytosis.
“In animal models of AD, tideglusib reduces tau phosphorylation, Aβ plaque burden, memory deficits, cell death and astrocytosis118,119.”
From Tau-targeting therapies for Alzheimer disease (2018) · cites this paper as [119]
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- Authors
- Serenó, L., Coma, M., Rodríguez, M., Sánchez-Ferrer, P., Sánchez, M. B., Gich, I., Agulló, J. M., Pérez, M., Avila, J., Guardia-Laguarta, C., Clarimón, J., Lleó, A., & Gómez-Isla, T.
- Affiliations
- Universitat Autònoma de Barcelona (ES)
- Centro de Biología Molecular Severo Ochoa (ES)
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2009-09
- Volume
- 35
- Issue
- 3
- Pages
- 359-367
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2049146362
- Cited by
- 368
- References
- 34
- Citations by year
- 2026: 16 · 2025: 25 · 2024: 22 · 2023: 21 · 2022: 18 · 2021: 28 · 2020: 32 · 2019: 16 · 2018: 27 · 2017: 20 · 2016: 15 · 2015: 16 · 2014: 30 · 2013: 20 · 2012: 22
- FWCI
- 13.92
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, GSK-3β inhibition, tau hyperphosphorylation, amyloid plaques, amyloid precursor protein, neurofibrillary tangles, neuronal cell death, entorhinal cortex, hippocampal CA1, memory impairment, astrocyte proliferation, double transgenic mice, therapeutic target
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Alzheimer Disease, Amyloid, Animals, Astrocytes, Enzyme Inhibitors, Female, Hippocampus, Humans, Male, Memory, Memory Disorders, Mice, Transgenic, Neurons, Receptors, Cell Surface, Space Perception, Thiadiazoles, Amyloid beta-Protein Precursor, tau Proteins, Cell Death, Entorhinal Cortex, Glycogen Synthase Kinase 3, Mice, Protease Nexins
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