The dysregulation of glucose metabolism in AD has gained importance as a therapeutic target because the administration of hormones that stimulate glucose metabolism, such as insulin and glucagon-like peptide 1 (GLP-1), improves cognitive responses in humans diagnosed with AD, as well as in mouse models of AD (Craft et al., 2012; Chapman et al., 2013; Freiherr et al., 2013), suggesting that the dysregulation of glucose in the brain could be critical in the onset and progression of AD as well as the progression of other metabolic diseases including diabetes. This evidence concerns the gene INS and metabolic disease.