A rising concentration of Aβ in the brain is a critical factor in the development of late-onset sporadic AD, playing a key role in triggering the “amyloid cascade.” Although transgenic models, such as amyloid protein precursor (APP)- and presenilin-1 (PS-1)-overexpressing models are known to be useful in the study of genetic aspects of early-onset AD (Ohno et al., 2004, 2007), the late-onset sporadic form of the disease, that accounts for approximately 90% of all cases (Bekris et al., 2010), requires unique approaches to model this form of AD. This evidence concerns the gene APP and Alzheimer disease.