Relatedly, many of the most widely used mouse models are based on the genetics of familial early‐onset AD (EOAD) where transgenic approaches were used to over‐express human sequences carrying mutations in amyloid precursor protein (APP) and/or presenilin (PSEN1, PSEN2), which represent only about 5% of AD patients.5, 6. The gene discussed is PSEN1; the disease is Alzheimer disease.