Using hypothesis-driven screening tests, we found that aging, upregulation of glycogen synthase kinase 3β (GSK-3β), a key kinase involved in Aβ production, tau hyperphosphorylation, and long-term synaptic inhibition seen in both AD and T2DM (Plattner et al., 2006; Yi et al., 2018), ApoE ε4 genetype, and olfactory dysfunction contributed to cognitive decline in T2DM patients (Xu et al., 2016). Here, APOE is linked to Alzheimer disease.