Moreover, SE caused hyperphosphorylation of tau at Ser202/Thr205 (AT8) at PSD, which is an early hyperphosphorylated site in Alzheimer’s disease,55,56 mediated by phosphorylation of CDK5 and GSK3β by Fyn.57 For Fyn to phosphorylate tau, Fyn must be in an active configuration.52,58 As shown in our previous studies27,28 and in this study, seizures increase Fyn activation (pSFK-Y416), which likely exposes its SH3 domains for tau interaction at PxxP5/6. This evidence concerns the gene FYN and early-onset autosomal dominant Alzheimer disease.