The upstream molecule in AD pathogenesis is beta-amyloid (A-B) protein [18]. DS patients present with AD-like pathogenesis in the early 40s compared to sporadic patients [19]. This is because of a 1.5-fold higher amyloid precursor protein (APP) expression in DS patients, which results in a 1.5-fold increase in A-B production [19]. Mapping the APP gene, which encodes for A-B, takes us to chromosome 21, and DS is caused by the third copy of chromosome 21 [20,21]. Thus this increase in gene dosage is the biggest neuropathogenic culprit in AD and DS patients [20]. This evidence concerns the gene APP and Dravet syndrome.