Collective findings suggested that pTau accumulation may be only one of many consequences stemming from ApoER2-Dab1 pathway disruption, and formed the basis for a unifying AD model that integrates pTau lesions with other hallmark (ApoE, amyloid β (Aβ), ApoJ) and emerging (Reelin, Dab1, pP85αTyr607, pPSD95Thr19) neuropathological features. This evidence concerns the gene DAB1 and Alzheimer disease.