The mechanism of the formation of Aβ aggregates in AD was dependent on the endocytosis of the APP through YTSI, the motif that promotes early endosome formation, which positively regulated this process by binding to APP tail 1a (PAT1a) and subsequent overexpression of RME-6, which was an activator of Rab5 [79]. This evidence concerns the gene RAB5A and Alzheimer disease.