For instance, neuronal Fe export is reliant upon the highly-abundant multi-copper oxidase ceruloplasmin,36 and genetic ablation of the ceruloplasmin gene in mice stimulates neuronal Fe overload and concurrent parkinsonism.37 Using our protocol, we would be able to identify voxels corresponding to reduced Cu and elevated Fe levels to produce a brain-wide picture of the effects of ceruloplasmin deficiency, and we could explore whether these effects are confined to vulnerable brain regions or are a system-wide phenomenon. This evidence concerns the gene CP and Parkinsonism.