There are also reports of age-dependent reductions in ZnT3 expression and synaptic Zn2+ levels in the hippocampal mossy fibers of human amyloid precursor protein-transgenic (Tg2576) mice, suggesting that extensive modifications of the brain’s Zn2+ pool, particularly synaptic (vesicular) Zn2+, underlie the neuronal dysfunction characteristic of Alzheimer’s disease (Lee et al., 2012). This evidence concerns the gene SLC30A3 and Alzheimer disease.