To this end, we utilized two different AD mouse models – the APP/PS1 double transgenic mice expressing mutant human APP protein (Mo/HuAPP695swe) and mutant human presenilin 1 (PS1-dE9), which is a widely used model for amyloid deposition and behavioral analysis (Radde et al., 2006; Serneels et al., 2009; Webster et al., 2013), and the PS19 tauopathy mouse model, which is known to exhibit severe neuronal loss and memory deficits at relatively young age (6–12 months old) (Takeuchi et al., 2011; Yoshiyama et al., 2007). This evidence concerns the gene APP and Alzheimer disease.