In view of our results, it becomes inviting to hypothesize that triplication of BACE2 may be the cause of the delayed onset of dementia in 30% of people with DS compared with DupAPP [7], and (because of the predicted abundance of BACE2 mRNA in endothelial cells) also the cause of a significantly lower degree of cerebral amyloid angiopathy (CAA) in the brains of people with DS compared with those of DupAPP [44]. This evidence concerns the gene BACE2 and dementia.