SLC2A1 and Alzheimer disease: Indeed, AD is also characterized by early reductions in glucose transport associated with diminished GLUT1 expression in brain endothelial cells, leading to BBB breakdown and cognitive dysfunction.[125] Therefore, pharmacological restoration of LRP1 or GLUT1 expression may increase LRP‐1‐mediated efflux of Aβ clearance, representing a novel strategy for AD therapy.