Our findings of the basal endogenous levels of Sox2, Oct4, and Nanog between the three fibroblast origins displayed a higher than two-fold decrease in Sox2 and Nanog levels in AD fibroblasts in comparison to the young and aged groups, while Oct4 levels similarly showed a declining pattern from young and aged to AD (Figure 2A–C). This evidence concerns the gene POU5F1 and Alzheimer disease.