ZnT3 knockout mice displayed an age-dependent deficit in cognition (Adlard et al., 2010), while mice overexpressing APP, but lacking ZnT3, appeared to have lower levels of synaptic zinc and a reduced plaque burden (Lee et al., 2002), implicating the contribution of synaptic zinc to the deposition of amyloid plaques in AD. The gene discussed is APP; the disease is Alzheimer disease.