When considered together with evidence from model systems that ApoER2-Dab1 signaling suppresses Tau phosphorylation,[54–57] these findings lend support to our unifying model wherein ApoER2 disruption could be a shared molecular origin linking ApoE, ApoJ, Reelin and Dab1 to the Aβ plaques and pTau tangles that define AD in humans (reviewed in [25, 27, 58]). Here, CLU is linked to Alzheimer disease.