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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
Y., Hong, K.-H., Kim, D
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GHK-CU has been studied for its involvement in redox regulation and extracellular matrix remodeling through copper-dependent mechanisms
Astrocyte senescence and Alzheimers disease: a review
