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

Grants

Funding Acknowledgements

The research in this study was supported through funds from the Australian National Health and Medical Research Council (NHMRC; grant number 1061550), the Motor Neurone Disease Research Institute of Australia (the Betty Laidlaw MND Research Grant), the Sigrid Juselius Foundation and the University of Melbourne.