This mechanism has a pathogenic role, as we observed a significant reduction of SAP97 phosphorylation in AD patients, which can be responsible for the previously reported defect in ADAM10 synaptic trafficking and activity.7 Finally, we showed that ADAM10 trafficking implies transit through dendritic Golgi outposts where ADAM10/SAP97 complex formation occurs. Here, DLG1 is linked to Alzheimer disease.