Our present results as well as others [23] indicate that the facilitation of Aβ production, which is accompanied by increases in the intermittent β-cleaved C-terminal fragment C99 resulting from elevated BACE1 and APP expression, may account for the exacerbation of Aβ accumulation in brains of STZ-induced diabetic AD transgenic mice. This evidence concerns the gene BACE1 and Alzheimer disease.