To reduce risk of copper toxicity from chronic CuATSM treatment [31]we therefore treated SOCK mice with either 15 mg/kg CuATSM or vehicle (n = 10/treatment) each day from weaning until 5.5 months-of-age to examine whether CuATSM could mitigate age-associated development of Parkinson-like wild-type SOD1 pathology, which is present by 6 weeks of age [15]. The gene discussed is SOD1; the disease is Parkinsonism.