Immunohistochemistry experiments demonstrating the increased intensity of proteasomal markers (Proteasome 20 S) suggest a potential enhancement in ubiquitin-dependent APP degradation following the overexpression of LV-FBXL16 in AD mice, as depicted in Fig. 7A. As shown in Fig. 7B, ubiquitination increased significantly in the mouse brain region overexpressing LV-FBXL16, whereas the level of APP decreased compared with that of the LV-GFP control, indicating that FBXL16 is necessary for ubiquitination-mediated APP clearance. Here, FBXL16 is linked to Alzheimer disease.