AD patients have been shown to have mildly increased levels of cortisol when compared to controls (Table 2) [34, 35] and corticosteroids have been shown to be able to induce Aβ plaque load and hyperphosphorylated tau levels in APP overexpressing mouse models [36–39], effects that were able to be reduced with a glucocorticoid receptor (GR) antagonist [40]. Here, NR3C1 is linked to Alzheimer disease.