Alzheimer's Disease, the 6th leading cause of US deaths, is characterized by amyloid-beta(Aβ) plaques and trace metal level imbalances. How this interaction occurs on the molecular level is currently unknown. Protein HSP-16.2 is known to interact individually with Cu,Zn,and Aβ, but their combined interaction has not yet been researched. I hypothesize that HSP-16.2 is involved in the binding of Aβ to Cu and Zn and increases in the levels of one trace metal cause increases in Aβ and other metals.