ArticleBrain communications2024
Enhanced Fyn-tau and NR2B-PSD95 interactions in epileptic foci in experimental models and human epilepsy.
Article in Brain communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Tau pathology in epilepsy: emerging mechanisms and translational opportunities.Brain : a journal of neurology · 2026Review
- Current review on inducible nitric oxide synthase and Src tyrosine kinase inhibitors as disease-modifiers in preclinical models of epilepsy.Histology and histopathology · 2026Review
- Differences in Neurofilament Light Chain, Glial Fibrillary Acidic Protein, and Tau Protein Levels in Patients with Temporal Lobe Epilepsy and Comorbid Depression.Molecular neurobiology · 2026Article
- Tau accumulation increases the susceptibility to effective seizures of electroconvulsive therapy.Translational psychiatry · 2026Article
- 8-Hydroxy-2-Anilino-1,4-Naphthoquinone Prevents Against Ferroptotic Neuronal Death and Kainate-Induced Epileptic Seizures.Pharmaceutics · 2025Article
- Mitigating organophosphate nerve agent, soman (GD), induced long-term neurotoxicity: Saracatinib, a Src Tyrosine Kinase inhibitor, as a potential countermeasure.Journal of neuroinflammation · 2025Article
- Diet-incorporated saracatinib, a Src tyrosine kinase inhibitor, counteracts diisopropylfluorophosphate (DFP)-induced chronic neurotoxicity in the rat model.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Bursts of brain erosion: seizures and age-dependent neurological vulnerability.Trends in molecular medicine · 2025Review
- The Effects of NeuronalCells · 2025Article
- Fyn, an important molecule in the brain, is a potential therapeutic target for brain tumours.Frontiers in pharmacology · 2024Review
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11 authors.
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Abstract
Epilepsy and Alzheimer's disease share some common pathologies such as neurodegeneration, seizures and impaired cognition. However, the molecular mechanisms of these changes are still largely unknown. Fyn, a Src-family non-receptor tyrosine kinase (SFK), and its interaction with tau in mediating brain pathology in epilepsy and Alzheimer's disease can be a potential therapeutic target for disease modification. Although Fyn and tau pathology occurs in both Alzheimer's disease and epilepsy, the dynamics of Fyn-tau and PSD95-NR2B interactions affected by seizures and their impact on brain pathology in epilepsy have not been investigated. In this study, we demonstrate a significant increase of Fyn-tau interactions following seizure induction by kainate in both acute and chronic rodent models and in human epilepsy. In the early phase of epileptogenesis, we show increased Fyn/tau/NR2B/PSD95/neuronal nitric oxide synthase complexes after status epilepticus and a postsynaptic increase of phosphorylated tau (pY18 and AT8), Fyn (pSFK-Y416), NMDAR (pNR2B-Y1472) and neuronal nitric oxide synthase. Hippocampal proximity ligation assay and co-immunoprecipitation revealed a sustained increase of Fyn-tau and NR2B-PSD95 complexes/binding in rat chronic epilepsy at 3 months post-status epilepticus. Enhanced Fyn-tau complexes strongly correlated with the frequency of spontaneously recurring convulsive seizures and epileptiform spikes in the chronic epilepsy model. In human epileptic brains, we also identified increased Fyn-tau and NR2B-PSD95 complexes, tau phosphorylation (pY18 and AT8) and Fyn activation (pSFK-Y416), implying the translational and therapeutic potential of these molecular interactions. In
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