Indeed, this approach already enabled us to show that (i) rare variations in the SORL1 gene might be responsible of a subset of AD-EOAD families [43] or at least constitute a penetrant risk factor for familial EOAD [44] and (ii) a set of genes defining an Aβ-centered genetic network are enriched in de novo mutations in sporadic cases [20]. This evidence concerns the gene SORL1 and Alzheimer disease.