Some of the pathogenic full-length as well as truncated mutant SOD1 proteins are known to exhibit distinct electrophoretic mobilities from that of the wild-type protein [48]; therefore, more biochemical analysis on tissue samples from SOD1-ALS patients will reveal any involvement of wild-type SOD1 in the abnormal accumulation of SOD1 proteins in spinal cord. Here, SOD1 is linked to amyotrophic lateral sclerosis.