Cellular prion protein acts as mediator of amyloid beta uptake by caveolin‐1 causing cellular dysfunctions in vitro and in vivo

Abstract

PrP^C expression adversely affects lifespan and behavior in 5xFAD mice. PrP^C increases Aβ1-40 and Aβ1-42 levels and Aβ-plaque load in 5xFAD mice. Cav-1 interacts with both PrP^C and Aβ peptides. Knocking out Cav-1 leads to a significant reduction in intracellular Aβ levels.