Morley and colleagues (2012[68]) demonstrated the direct effects of amylin on cognition and AD pathogenesis by showing the effects of pramlintide on memory in senescence-accelerated prone (SAMP8) mouse (model of sporadic AD), the results indicated reduced expression of HO-1 (cellular stress protein that is activated during high oxidative stress and inflammatory states). This evidence concerns the gene IAPP and Alzheimer disease.