SOD1 and amyotrophic lateral sclerosis: Irrelevant of the underlying cause, we speculate that impaired ER-golgi trafficking may promote cytoplasmic disordered wild-type SOD1 accumulation in motor neurons of non-SOD1-fALS and sALS patients [29], constituting a common pathway leading to neurotoxic cytoplasmic SOD1 pathology in all ALS subgroups examined in this study.