Preclinical studies clearly show how chronic Cu exposure increases non-ceruloplasmin Cu in plasma and in brain capillaries [91,93], mimicking non-ceruloplasmin Cu excess noted in AD patients [94] and, particularly, in a subset of AD patients [83], which is typified by non-ceruloplasmin Cu levels higher than 1.6 μmol/L and susceptibility to Cu disturbances on a genetic basis [81,95]. The gene discussed is CP; the disease is Alzheimer disease.