It is increasingly recognized that APOE ε4 may interact with obesity to augment disruptions in lipid, glucose, insulin, and immune response metabolism and that such adverse interactions may increase the vulnerability of medial temporal lobe structure to neurodegeneration (Jones and Rebeck, 2018; Mole et al., 2020; Zade et al., 2013). This evidence concerns the gene APOE and obesity due to melanocortin 4 receptor deficiency.