ArticleNeuromolecular medicine2023
Tau and GSK-3β are Critical Contributors to α-Synuclein-Mediated Post-Stroke Brain Damage.
Article in Neuromolecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Gut bacterial metabolite imidazole propionate potentiates Alzheimer's disease pathology.Nature communications · 2026Article
- Alpha-Synuclein Dynamics in Cerebral Ischemia.ASN neuro · 2026Review
- Identification of Novel Scaffolds Against GSK-3β for Targeting Alzheimer's Disease Through Molecular Modeling Techniques.Cellular and molecular neurobiology · 2025Article
- Anti-oxidant activity of coenzyme Q10 against AlClToxicology research · 2024Article
- Article
- The contribution of β-amyloid, Tau and α-synuclein to blood-brain barrier damage in neurodegenerative disorders.Acta neuropathologica · 2024Review
- Article
- Alpha-, Beta-, and Gamma-Secretase, Amyloid Precursor Protein, and Tau Protein Genes in the Hippocampal CA3 Subfield in an Ischemic Model of Alzheimer's Disease with Survival up to 2 Years.Journal of Alzheimer's disease : JAD · 2024Article
- Article
- Preservation of Biomarkers Associated with Alzheimer's Disease (Amyloid Peptides 1-38, 1-40, 1-42, Tau Protein, Beclin 1) in the Blood of Neonates after Perinatal Asphyxia.International journal of molecular sciences · 2023Article
- Value of plasma alpha- and beta-synuclein levels in the diagnosis, severity, and functional outcome of acute ischemic stroke.Turkish journal of emergency medicineArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Post-stroke secondary brain damage is significantly influenced by the induction and accumulation of α-Synuclein (α-Syn). α-Syn-positive inclusions are often present in tauopathies and elevated tau levels and phosphorylation promotes neurodegeneration. Glycogen synthase kinase 3β (GSK-3β) is a known promoter of tau phosphorylation. We currently evaluated the interaction of α-Syn with GSK-3β and tau in post-ischemic mouse brain. Transient focal ischemia led to increased cerebral protein-protein interaction of α-Syn with both GSK-3β and tau and elevated tau phosphorylation. Treatment with a GSK-3β inhibitor prevented post-ischemic tau phosphorylation. Furthermore, α-Syn interaction was observed to be crucial for post-ischemic GSK-3β-dependent tau hyperphosphorylation as it was not seen in α-Syn knockout mice. Moreover, tau knockout mice show significantly smaller brain damage after transient focal ischemia. Overall, the present study indicates that GSK-3β catalyzes the α-Syn-dependent tau phosphorylation and preventing this interaction is crucial to limit post-ischemic secondary brain damage.
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Registered trials
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