LRP1 and Alzheimer disease: Given the already weak interaction of Aβ–bApoE ε4 compounds with endothelial LRP1 (Path II), the additional LRP1 loss and elevated MMP9 release (Cycle B) further increase Aβ accumulation contributing to the formation of toxic Aβ oligomers and plaques [29,31], which finally promote inflammatory and neurodegenerative processes related to AD [3,7,27,28].