BACE1 and Alzheimer disease: Other studies have also demonstrated that sleep deprivation or restriction in various AD models exacerbates AD-related biochemical or pathological changes in mice brains, such as an increase in Aβ or phosphorylated tau [32,33], an increase in insoluble phosphorylated tau and glial fibrillary acidic protein levels [34], and an increase in Aβ40, Aβ42 and β-site amyloid-precursor-protein-cleaving enzyme 1 (BACE1), which produce toxic Aβ species [35].