β-Amyloid efflux mediated by p-glycoprotein

摘要: A large body of evidence suggests that an increase in the brain β-amyloid (Aβ) burden contributes to etiology Alzheimer's disease (AD). Much is now known about intracellular processes regulating production Aβ, however, less regarding its secretion from cells. We report p-glycoprotein (p-gp), ATP-binding cassette (ABC) transporter, Aβ efflux pump. Pharmacological blockade p-gp rapidly decrease extracellular levels secretion. In vitro binding studies showed addition synthetic human Aβ1–40 and Aβ1–42 peptides hamster mdr1-enriched vesicles labeled with fluorophore MIANS resulted saturable quenching, suggesting both interact directly transporter. Finally, we were able measure transport across plasma membranes enriched vesicles, this phenomenon was ATP- p-gp-dependent. Taken together, our study a novel mechanism detachment cellular membranes, represents obvious route towards identification such brain.