This robust AD mouse model develops severe amyloid pathology and cognitive decline at an early age through high expression of three familial mutant types of human amyloid precursor protein (hAPP; Swedish, Florida, and London) and two mutant forms of presenilin (PSEN1; M146L and L286V).26 Overall, our studies establish strong experimental evidence for an in vivo link between metal–Aβ and AD development, implying that targeting metal–Aβ complexes could be an effective strategy for the future development of new therapeutics. Here, APP is linked to Alzheimer disease.