Since these authors observed the same upregulation in MAM function and ER mitochondrial communication in fibroblasts from patients with sAD, without mutations in PSEN1, PSEN2, and APP, they suggested that MAM-upregulated function is a common feature in both fAD and sAD, and proposed that it may represent a pathogenic initiator of AD [160,161]. The gene discussed is PSEN1; the disease is familial Alzheimer disease.