Consistent evidence from human studies and animal studies has revealed abnormal glucose metabolism in the brain that could occur prior to AD pathology and cognitive impairment, including reduced GLUT1 and GLUT3 [54,55], impaired insulin signaling [56,57], aberrant glucose metabolism [58,59,60], mitochondrial dysfunction and reduced ATP synthesis [61,62]. The gene discussed is SLC2A1; the disease is Alzheimer disease.