Abstract
To clarify how Aβ deposits induce secondary tauopathy, the presence of phosphorylated tau, glycogen synthase kinase 3α (GSK3α), GSK3β, cyclin-dependent kinase 5 (CDK5), mitogen-activated protein kinase (MAPK) and fyn were examined in the Tg2576 brain showing substantial brain Aβ amyloidosis and behavioral abnormalities. Phosphorylated tau at Ser199, Thr231/Ser235, Ser396 and Ser413 accumulated in the dystrophic neurites of senile plaques. The major kinase for tau phosphorylation was GSK3β. Smaller contributions of GSK3α, CDK5 and MAPK were suggested. Thus, brain Aβ amyloidosis has a potential role in the induction of tauopathy leading to the mental disturbances of Alzheimer's disease.
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