Although multiple studies have suggested a role for alterations of zinc (Zn) and zinc
transport (ZnT) proteins in the pathogenesis of Alzheimer's disease, the exact role of this
essential trace element in the progression of the disease remains unclear. The following
review discusses the normal role of Zn and ZnT proteins in brain and the potential effects of
their alteration in the pathogenesis of Alzheimer's disease, particularly in the processing of
the amyloid-β protein precursor and amyloid-β peptide generation and aggregation.