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However, the mechanisms leading to the accumulation of A oligomers in sporadic AD are not clear

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Importantly, Cu II (atsm) treatment improves Cu delivery to SOD1 in mutant SOD1 transgenic mice and improves survival time despite eliciting an increase in the total amount of mutant SOD1 protein present, [151] suggesting SOD1mediated mitochondrial dysfunction is closely tied to SOD1 Cu metalation rather than the amount of SOD1 protein