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The accumulation of enzymatically inactive cuproenzymes is a CNS-specific phenomenon of the SOD1 G37R mouse model of ALS and can be restored by overexpressing the human copper transporter hCTR1
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15 We also conducted a separate analysis to evaluate the efficacy of more general treatment types by pooling the treatment nodes with similar mechanisms (eg, oral antibiotics, topical antibiotics, topical retinoids)
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