One of the main pathological hallmarks in APP/PS1 mice, the deposition of amyloid-β plaques, was found unchanged after the treatment with GW2580, as evidenced by multiplex analysis of soluble amyloid-β38, amyloid-β40and amyloid-β42(Fig. 6A), 6E10 immunostaining (Figs 6B and7C) and Congo Red staining (not shown), suggesting a requirement for microglial proliferation/activation to associate the amyloidogenic component with the behavioural decline observed in Alzheimer’s disease-like pathology. This evidence concerns the gene APP and early-onset autosomal dominant Alzheimer disease.