During the course of AD, CAP can reduce Aβ formation through several mechanisms, including promoting the maturation of deintegrin and metalloproteinase 10 (ADAM 10), shifting the direction of amyloid precursor protein (APP) cleavage and blocking the formation of Aβm, and ameliorating Aβ pathology through AKT/GSK-3β-mediated Nrf2 activation, which achieves protective effects [42,43]. This evidence concerns the gene AKT1 and Alzheimer disease.