While the etiology of Alzheimer's disease (AD) is complex and not fully understood, genetic mutations provide compelling evidence that the amyloid beta (Aβ) peptide plays a critical role in AD pathogenesis.1,2 Indeed, mutations in the genes encoding either the Aβ progenitor (i.e. the amyloid precursor protein or APP) or the APP processing enzyme (presenilin 1 and 2 genes) are sufficient to cause AD.1 Moreover, none of the familial AD mutations involve genes encoding for the tau protein. Here, PSEN1 is linked to Alzheimer disease.