The greater alteration observed in AD mice than in WT mice, regardless of whether they were injected with LV-GFP or LV-FBXL16, this might suggest that the presence of AD pathology, and the subsequent intervention through FBXL16 overexpression create a condition in which the potential for cognitive improvement is more substantial than that in normal aging mice. This evidence concerns the gene FBXL16 and Alzheimer disease.