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Biochemistry 57:20592060 Mizuno A, Toyama T, Ichikawa A, Sakai N, Yoshioka Y, Nishito Y, Toga R, Amesaka H, Kaneko T, Arisawa K et al (2023) An efficient selenium transport pathway of selenoprotein P utilizing a high-affinity ApoER2 receptor variant and being independent of selenocysteine lyase

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According to this scenario, a catalytically inactive SOD1 mutant may act as a prion-like transmitter of the misfolding signal to efficiently spread the pathology, whereas the neurotoxic effect per se is caused by the ubiquitous SOD1 WT , the structural and catalytic properties of which compromised by its interaction with the misfolded SOD1 mutant