ArticleFrontiers in cellular neuroscience2020
GSK3β and Tau Protein in Alzheimer's Disease and Epilepsy.
Article in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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91 citing papers in PubMed, 144 citations in OpenAlex.
- Current Landscape of Glycogen Synthase Kinase-3β PET Tracers: Progress, Limitations, and Perspectives-A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Restoration of Neuronal Metabolism and Memory in Alzheimer's Disease by Reprogramming the Exosomal microRNA Network.Journal of molecular neuroscience : MN · 2026Review
- Mitochondrial Dysfunction in Alzheimer's Disease and Mitochondria-Targeted Therapeutics.Cells · 2026Review
- Corneal Immune Cell Alterations and Tau Pathology in a Mouse Model of Alzheimer's Disease.Investigative ophthalmology & visual science · 2026Article
- Tau accumulation increases the susceptibility to effective seizures of electroconvulsive therapy.Translational psychiatry · 2026Article
- Reticulocalbin-2 in the Hippocampus Improves Cognitive Function of Diabetic Mice.Brain and behavior · 2026Article
- Transcriptome-informed metabolic modeling reveals astrocyte-specific vulnerabilities in mild cognitive impairment and Alzheimer's disease progression.Frontiers in bioinformatics · 2026Article
- Alzheimer's Disease: From Molecular Pathogenesis to Disease-Modifying Therapies and Clinical Implementation in Aging Populations.Clinical interventions in aging · 2026Review
- Reduced BOLD-CSF coupling as a potential functional imaging correlate of semantic fluency decline in MRI-negative temporal lobe epilepsy.Frontiers in aging neuroscience · 2026Article
- Insulin resistance and cognitive decline: the metabolic mechanisms linking type 2 diabetes to Alzheimer's disease.Diabetology international · 2025Review
- Integrated computational approaches for identification of potent pyrazole-based glycogen synthase kinase-3β (GSK-3β) inhibitors: 3D-QSAR, virtual screening, docking, MM/GBSA, EC, MD simulation studies.Molecular diversity · 2025Article
- The Inflammatory Bridge Between Type 2 Diabetes and Neurodegeneration: A Molecular Perspective.International journal of molecular sciences · 2025Review
- Neuroprotective Role of Omega-3 Fatty Acids: Fighting Alzheimer's Disease.Molecules (Basel, Switzerland) · 2025Review
- Tau phosphorylation at Alzheimer's disease biomarker sites impairs its cleavage by lysosomal proteases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Elucidation of Artemisinin as a Potent GSK3β Inhibitor for Neurodegenerative Disorders via Machine Learning-Driven QSAR and Virtual Screening of Natural Compounds.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Zebrafish metabolomics: a comprehensive approach to understanding health and disease.Functional & integrative genomics · 2025Review
- Toxoplasma GRA16 attenuates Tau hyperphosphorylation and enhances autophagy in thrombin-treated HT-22 hippocampal neuronal cells.Scientific reports · 2025Article
- Trace amine-associated receptor 1 (TAAR1): an emerging therapeutic target for neurodegenerative, neurodevelopmental, and neurotraumatic disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Nootropic foods in neurodegenerative diseases: mechanisms, challenges, and future.Translational neurodegeneration · 2025Review
- Multi-target approach to Alzheimer's disease prevention and treatment: antioxidant, anti-inflammatory, and amyloid- modulating mechanisms.Neurogenetics · 2025Review
31 more citing papers are in PubMed but not listed here.
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4 authors at 3 institutions in 1 country.
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Abstract
Alzheimer's disease (AD) is the most common form of dementia present in older adults; its etiology involves genetic and environmental factors. In recent years, epidemiological studies have shown a correlation between AD and chronic epilepsy since a considerable number of patients with AD may present seizures later on. Although the pathophysiology of seizures in AD is not completely understood, it could represent the result of several molecular mechanisms linked to amyloid beta-peptide (Aβ) accumulation and the hyperphosphorylation of tau protein, which may induce an imbalance in the release and recapture of excitatory and inhibitory neurotransmitters, structural alterations of the neuronal cytoskeleton, synaptic loss, and neuroinflammation. These changes could favor the recurrent development of hypersynchronous discharges and epileptogenesis, which, in a chronic state, favor the neurodegenerative process and influence the cognitive decline observed in AD. Supporting this correlation, histopathological studies in the brain tissue of temporal lobe epilepsy (TLE) patients have revealed the presence of Aβ deposits and the accumulation of tau protein in the neurofibrillary tangles (NFTs), accompanied by an increase of glycogen synthase kinase-3 beta (GSK3β) activity that may lead to an imminent alteration in posttranslational modifications of some microtubule-associated proteins (MAPs), mainly tau. The present review is focused on understanding the pathological aspects of GSK3β and tau in the development of TLE and AD.
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