In this study, we compared the abilities of 50% BACE1 reduction with heterozygous gene deletion to suppress β-amyloidogenesis and AD-like phenotypes in the 5XFAD transgenic mouse model at earlier (6-month-old) and advanced (15–18-month-old) stages, which show normal and increased levels of BACE1 expression in brains, respectively. This evidence concerns the gene BACE1 and Alzheimer disease.