In agreement with defective degradation of dysfunctional mitochondria, we noticed unchanged level of the mitophagy priming protein PINK1 in mitochondria fraction of vehicle- or with γ-secretase inhibitor-treated 3xTgAD mice (Fig. 7f, h), and enhanced HSP10 protein level in 3xTg-AD mice versus WT mice (Fig. 7f, h), and observed a significant enhancement of TIMM23, HSP10, and MFN2 protein levels in 3xTg-AD versus WT mice treated with γ-secretase inhibitor (Fig. 7f, h). This evidence concerns the gene HSPE1 and Alzheimer disease.