IAPP and Alzheimer disease: Figure 2 shows our hypothesis that abundant Aβ, in either monomeric, oligomeric or fibriller form, in the AD brain may block the ability of amylin to bind to its receptor and interefere with normal amylin functions in the brain; giving exogenous amylin class peptides could rescue the amylin activities in the brain as well as removing Aβ out of the brain.