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Many factors are involved in tau phosphorylation and aggregation in patients with Alzheimer’s disease (AD) and in the transgenic mouse model expressing human mutant amyloid precursor protein. The present study examined the role of tau phosphorylation and aggregation in AD neuropathology using mouse astrocytes. A-3825, a novel pyrido[2,1-b]quinazolin-5(4H)-one derivative, showed a potent suppressive effect on tau phosphorylation and aggregation. Thus, in this study, the effects of A-3825 on tau phosphorylation and aggregation in human astrocytes were examined, and the inhibitory mechanisms of A-3825 in the cell culture system were examined. Tau and glycogen synthase kinase 3beta (GSK3beta) were co-immunoprecipitated with tau. The results showed that A-3825 suppressed tau phosphorylation at multiple sites, including Ser396/404 and Ser262/356/396/404. Accordingly, A-3825 suppressed tau-induced hyperphosphorylation of phosphorylated p90RSK (Thr359/Ser363/Thr410) and GSK3beta (Ser9). In addition, A-3825 suppressed tau aggregate formation. A-3825 did not decrease the total levels of tau and GSK3beta; therefore, the suppression of hyperphosphorylation of tau and of tau aggregation was

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