Further studies in the 3×TG AD mice revealed an increased CNS uptake which was not accounted for by altered BBB integrity or changes in vascular space in the AD model mice, as there were no differences in [14C]sucrose uptake between the two groups; and neither was it explained by non-expression of the transporters studied (P-gp, OCT1, OCT2, OCT3, OCTN1, OCTN2, MATE1, MATE2 and PMAT). This evidence concerns the gene SLC22A1 and Alzheimer disease.