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[203b] however, treatment of hSOD1 G93A /hCCS mice with the orally bioavailable Cu delivery agent diacetylbis(N(4)‐methylthiosemicarbazonato) Cu II (Cu II (atsm)) restored cytochrome c oxidase activity and significantly extended survival time, [154] suggesting Cu‐dependent mechanism(s) of mitochondrial dysfunction driven by misfolded SOD1 may indeed be present
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