HFD in mice induced acute reduction of glucose transporter 1 (GLUT1), which was then gradually restored upon prolonged HFD in parallel with compensatory upregulation of vascular endothelial growth factor (VEGF) by CD206+ macrophages at the BBB.64 Myeloid‐specific deletion of VEGF (VEGFalox/lox LysM Cre+/‐) impaired BBB‐GLUT1 expression, brain glucose uptake, and memory formation in obese mice, as well as exacerbated neuroinflammation and cognitive decline in APP‐PS1 mice. This evidence concerns the gene SLC2A1 and Mental deterioration.