SOD1 and amyotrophic lateral sclerosis: Based on the evidence of secretory pathway dysfunction in ALS, Turner et al. (2005) confirmed our previous researches related to SOD1 secretion also in mouse motoneuron like NSC-34 cells; in addition, these authors linked deficient extracellular accumulation of SOD1 mutants to intracellular aggregates and toxicity in NSC-34 cells demonstrating that extracellular delivery of human wt-SOD1 improved clinical disease in transgenic ALS rats.