Accordingly, it is interesting to note that the AD brain is not only widely reported to be deficient in Glut1 and hypometabolic – in 18F‐FDG PET imaging studies71, 72, 73, 74, 75 – but also appears hypoperfused.76, 77, 78, 79, 80, 81 Moreover, at least one study found an inverse correlation between CSF levels of the AD‐causing Aβ peptide and CSF glucose, suggestive of low concentrations of glucose in the CSF of patients with AD. Here, SLC2A1 is linked to Alzheimer disease.