Here we show that treatment of SOCK mice with the blood-brain-barrier-permeable copper delivery drug, diacetyl-bis(4-methylthiosemicarbazonato)copper(II) (CuATSM), mitigates the formation of Parkinson-like wild-type SOD1 pathology, increases SN dopamine neuron survival and improves motor function. The gene discussed is SOD1; the disease is Parkinson disease.