In addition, Cirrito et al. [19] reported that P-gp deficiency at the BBB increased amyloid-β deposition in a murine model of Alzheimer’s disease, suggesting that P-gp normally discharges Aβ out of the brain or periarterial interstitial fluid, and that perturbation of Aβ efflux directly affects Aβ accumulation within the brain or perivascular areas. This evidence concerns the gene PGP and early-onset autosomal dominant Alzheimer disease.