INS and type 2 diabetes mellitus: One or more possible explanations may be reasonable for the observed results: 1) glucose dysregulation in T2DM patients with cognitive dysfunction promotes adipsin production as a compensatory mechanism to maintain normal insulin secretion [17], that leads to compensatory IR, which, in turn may contribute to impairment of cellular insulin signaling [43], reduction of brain insulin uptake, and increased levels of Aβ [10].