This lack of Reelin accumulation in amygdala differed from the prominent extracellular Reelin deposits that we previously observed in the hippocampus and subiculum in a subset of these same MCI and AD cases.[27] Since Reelin signaling through ApoER2 regulates the degradation and phosphorylation status of neuronal ApoER2 signaling partners including Dab1, P85α and Tau respectively in preclinical models, this extracellular Reelin deposition in hippocampus suggests that disruption of Reelin-ApoER2 binding and internalization in hippocampus may play a role in AD pathogenesis. This evidence concerns the gene MAPT and Alzheimer disease.