As mentioned above, the cross-interaction and co-deposition of IAPP and Aβ were shown by numerous histological, in vivo animal models and in vitro studies to contribute to the pathological link between T2D and AD at the protein level; hence, preventing IAPP and Aβ cross-interaction, in addition to self-interaction, is a promising therapeutic strategy to address T2D-associated AD and vice versa. Here, IAPP is linked to Alzheimer disease.