In these regions, NE played very different roles for each of the two studied AEP targets, tau and APP, where NE deficiency increased AEP-tau and p-tau in a sleep-independent manner, while NE deficiency prevented the sleep-dependent (CFS) increase in AEP-APP and Aβ, demonstrating that NE critically determines the balance of Aβ and tau in AD-vulnerable brain regions across rested and sleep disruption conditions. This evidence concerns the gene APP and Alzheimer disease.