Although the precise nature of such metabolic improvement remains unknown, evidence suggests a role for the recovered neurovascular unit (involving a NF-κB-induced balance between the vasoconstrictor endothelin-1 and the vasodilator endothelial nitric oxide synthase (eNOS)) [84,85] and the normalization of (cerebral) blood flow on the increment of GLUTs levels and/or function (their loss, particularly of those at the blood-brain barrier, like GLUT1 and, to a lesser extent, GLUT4, constitutes an early event in AD pathology) [86,87]. This evidence concerns the gene NFKB1 and Alzheimer disease.