The aim of the present study is to extensively characterize AD-related alterations of platelet APP processing and secretion of sAPPβ, and to measure serotonin levels in three different mouse models: the hypercholesterolemia mouse model, the triple transgenic model displaying Aβ plaques and tau pathology at late stage, and the APP_SweDI mouse model showing Aβ plaques at an early stage, but no tau pathology. The gene discussed is APP; the disease is Alzheimer disease.