Furthermore, utilizing LAT1 as a brain- and astrocyte-targeted carrier is a feasible approach to treat AD, since we have reported earlier that neither AD-induced alterations of transgenic mice nor lipopolysaccharide- (LPS-) induced inflammation changes the expression or function of LAT1 at the BBB or primary astrocytes [29, 44]. Here, SLC7A5 is linked to Alzheimer disease.