During AD progression, BVR-A Tyr phosphorylation is reduced, and BVR-A nitration is increased due to the elevated oxidative stress, a process that impairs the activation of the insulin signaling pathway and promotes CK1-mediated BACE1 recycling at the plasma membrane, where BACE1 cleaves APP and leads to elevated Aβ production. Here, BACE1 is linked to Alzheimer disease.