Similar to our prior study, which showed disrupted sleep phenotypes depending on the level of Aβ deposition (33), we also observed that increased Aβ deposition in APPPS1:E4 male mice with AD-tau injection at 6 months of age was associated with decreased overall sleep percentages and increased sleep bout lengths as compared with APOE4-knockin (apoE4) male mice (Figure 9, G and H, and Supplemental Figure 5A and B). This evidence concerns the gene APOE and Alzheimer disease.