The major findings are: (1) the 48 h of hyperinsulinemic condition is enough to induce neuronal insulin resistance, increase neuronal apoptotic protein markers and AD markers, and augment the formation of extracellular plaques; (2) the 24 h liraglutide treatment restores neuronal insulin sensitivity and decreases the formation of AD markers and plaque formation, but is not enough to affect any changes in neuronal apoptotic markers and glucose uptake in the hyperinsulinemic condition; and (3) liraglutide suppresses BACE-1 activity which is accelerated under a hyperinsulinemic condition. This evidence concerns the gene BACE1 and Alzheimer disease.