APP and amyloidosis: Our studies in mammalian cell culture, Drosophila and mouse AD models, and post-mortem AD patient brain samples support the notion that the proper translation and biogenesis of APP.C99 depend on RQC activity, the inadequacy of which can result in ribosome collision  and accumulation of translationally stalled and CAT-tailed APP.C99 species that impair the endolysosomal and autophagy systems and seed the formation of amyloid plaques, causing proteostasis failure and AD pathogenesis.