GSK3B and Alzheimer disease: They found that an early, transient and site-specific GSK-3β-mediated tau overphosphorylation (3–6 h after NGF withdrawal) at two AD-relevant pathological epitopes (Ser262 and Thr231) is temporally and causally related with an activation of the endogenous amyloidogenic pathway in NGF-deprived hippocampal primary neurons [275].