These type 2 DM models show increased levels of Aβ and the β-secretase-cleaved C-terminal fragment of APP (β-CTF or C99, an intermediate β-metabolite of APP) concomitant with BACE1 elevations in the hippocampus and cerebral cortex, leading to learning and memory impairments (Zhang T. et al., 2009; Jiang et al., 2012). This evidence concerns the gene APP and memory impairment.