Pathophysiological studies show that APOE immunoreactivity exists in senile plaques, indicating a significant role of APOE in the metabolism of Aβ (Kim et al., 2009; Castellano et al., 2011), which is thought to initiate toxic events and further have distinct functions in regulating tau hyperphosphorylation, synaptic plasticity, cell signaling, lipid transport and metabolism, and neuroinflammation (Yu et al., 2014; Giau et al., 2015). The gene discussed is APOE; the disease is Senile plaques.