It is widely acknowledged that hyperglycemia-induced neurotoxicity primarily arises from high production of advanced glycation end (AGE) products, increased flux in the polyol pathway, activation of protein kinase C (PKC) isoforms, and augmented flux in the hexosamine pathway, all of which contribute to an augmentation in oxidative harm and vascular complications [32]. This evidence concerns the gene PRRT2 and Hyperglycemia.