INS and Alzheimer disease: A crosstalk between insulin cascade and AD manifestations has been highlighted earlier, where it was identified that Aβ, a surrogate marker of AD pathology, competitively inhibits the binding of insulin to its neuronal receptors48,49 and interferes with tyrosine phosphorylation/activation of IRS-150, while permitting its serine phosphorylation/inhibition to hinder GLUT 4 translocation15.