Fig. 1.

GSK3 and its role in AD. Over-activity of GSK3 caused either by aberrant Wnt or insulin signaling in sporadic AD cases or through familial mutations in PS or APP in FAD, might play an integral role in disease progression. GSK3 mediates the hyper-phosphorylation of tau, the increased production of Aβ from APP (via β and γ secretase-mediated cleavage) and results in impairments in learning and memory and could potentially heighten microglial-mediated inflammatory responses in the local vicinity of Aβ plaques.