Indeed, abnormal BACE1 activity is a key factor in AD pathogenesis, and this can be clearly observed in patients with trisomy 21 (i.e., Down Syndrome), where a marked increase in BACE1 is found to be the key contributor in the development of early-onset familial AD in this group [17]; thus, further supporting the potential of BACE1 as a target for AD. This evidence concerns the gene BACE1 and Alzheimer disease.