Nigral copper deficiency in Parkinson disease patients is associated with a down-regulation of the cellular copper import protein Ctr1 [13], and hence, our novel mouse model was created by crossbreeding mice expressing half the normal level of Ctr1 (termed Ctr1+/- mice), with transgenic mice overexpressing human wild-type SOD1 (termed hSOD1WT mice) (Fig. 2a). The gene discussed is SOD1; the disease is Parkinson disease.