A probable role for brain metabolic dysfunction in the pathogenesis of AD is further supported by the: 1) findings of cognitive impairment and neurodegeneration in experimental models of brain insulin/IGF resistance [6,49–53]; 2) halting or reversal of cognitive deficits by insulin, GLP-1 analog, or insulin sensitizer treatments in humans and experimental animals [18–27]; and 3) effectiveness of lifestyle changes for reducing insulin resistance and preserving cognition [54–57]. The gene discussed is GCG; the disease is Cognitive impairment.