Although these mouse models simulate several key aspects of human AD (Games et al., 1995; Hsiao et al., 1996; Sturchler-Pierrat et al., 1997; Götz et al., 2004; Cheng et al., 2007; Cissé et al., 2011; Verret et al., 2012), in these animals, Aβ and other APP fragments maybe overproduced and/or ectopically expressed (Chang and Suh, 2005; Mitani et al., 2012; Nicolas and Hassan, 2014; Kerridge et al., 2015; Nhan et al., 2015; Willem et al., 2015; Xia et al., 2016; Sasaguri et al., 2017). This evidence concerns the gene APP and Alzheimer disease.