INS and type 2 diabetes mellitus: This effect was partly attributed to (1) halting of T2DM-associated metabolic dysfunction, (2) modulation of the crosstalk between hippocampal insulin and noncanonical Wnt/β-catenin cassette, (3) stimulation of the canonical Wnt/β-catenin signaling pathway, (4) mitigation of neuroinflammation and preservation of BBB integrity, (5) improvement of memory and cognitive abilities, and 6) restoration of the hippocampal histological architecture.