In cerebral ischemia, inflammatory monocytes/macrophages (green) infiltrate the brain and polarize in the parenchyma to a protective phenotype (red). Hyperglycemia impairs noninflammatory polarization of macrophages. In monocytes/macrophages, AGER, the receptor for AGEs, inhibits polarization toward a protective phenotype. MG, an α-dicarbonyl derivative of glucose, reduces the expression and release of the cytokine CSF-1 from endothelial cells. The latter promotes the polarization of macrophages to a noninflammatory cell type.