SLC2A1 and Alzheimer disease: The combination of reduced glucose and a shrinking cerebral microvasculature may also explain amyloid deposition and the tau‐containing neurofibrillary tangles that serve as hallmarks of the AD brain.82 The cascade of events likely spirals into a vicious cycle, with amyloid deposition further damaging brain endothelia, exacerbating Glut1 deficiency, and damaging the brain capillary network.83 Arresting or reversing such pathology might be effected by augmenting Glut1.