Since postsynaptic proteins were less affected in patients, they were excluded here.18 The present meta-analysis, therefore, was aimed at characterizing presynaptic protein changes in AD models to i) examine which presynaptic protein changes occur in rodents, ii) how they relate to alterations found in human AD patients, and iii) establish a relationship between the decline of presynaptic proteins as a function of underlying pathology, e.g., tau or amyloid-β. The gene discussed is MAPT; the disease is Alzheimer disease.