Mouse models that express familial AD-associated mutations in genes coding for amyloid precursor protein and presenilin that increase amyloid levels in the brain or that express mutated Tau leading to neurofibrillary tangles provide an entry point to study mechanisms of synapse loss associated with prominent AD related pathologies, such as amyloid plaques and neurofibrillary tangles (Jankowsky and Zheng, 2017). The gene discussed is APP; the disease is Alzheimer disease.