Cognitive dysfunction and diabetes are parallel phenomenon arising from coincidental roots linked to various pathological changes such as alterations in anti-oxidants SOD, CAT, GST and enhancement of inflammatory markers TNF-α, IL-6, etc. In the brain, insulin receptor density is highest in the olfactory bulb, hypothalamus, hippocampus, cerebral cortex, striatum and cerebellum [29, 30] which mediates translocation of glucose transporter (GLUT-4) and regulate memory formation and other cognitive functions by activation of phosphorylated Gsk-3β, cAMP/CREB involved in cell survival. Here, GSK3B is linked to diabetes mellitus.