The toxic deposits of insoluble Aβ in the hippocampus and cortex promote the formation of neuritic senile plaques, and a neuron-Aβ interaction induces tau phosphorylation through tau kinase activation or by modulating phosphorylated state of tau, as seen in the primary septal and hippocampal neurons (Takashima et al., 1998; Zheng et al., 2002). The gene discussed is MAPT; the disease is Senile plaques.