Results from several other groups also support the idea that efflux of soluble Aβ does occur at the blood–brain barrier and that LRP1 is involved in this elimination.Jaeger et al. [461] showed that antisense oligonucleotides against LRP-1 substantially decreased the loss of Aβ1-42 after intraparenchymal injection.
Pflanzner et al. [462] demonstrated LRP1-dependent Aβ1-40 transport across monolayers of primary mouse brain capillary endothelial cells, a transport not observed in monolayers of cells with genetically modified LRP1.
Roberts et al. [457] confirmed that efflux of Aβ from brain to blood occurs in vivo by finding that the concentration in venous blood leaving the brain was 7.5% higher than that in arterial blood.
Qosa et al. [424] using the brain efflux index method found that 62% of added 125I-Aβ1-40 appeared in the blood.
Storck et al. [453] developed a mouse model in which LRP1 could be knocked out selectively in endothelial cells and showed that the knockout reduced the initial rate of loss of 125I-Aβ1-42 by 48%.