SOD1 and amyotrophic lateral sclerosis: Indeed, apparent amounts of SOD1 reactive to apoSOD, EDI, and UβB showed good linear correlations with those of C4F6 (R2 = 0.65, 0.75, and 0.59, respectively; Fig. 7a-c); in the plots, the data points on the non-ALS cases lacking the C4F6-reactive SOD1 were concentrated near the origin of the coordinates, while those on the ALS cases as well as the PDSOD1 and PSPSOD1 cases deviated from the origin with the highest intensity in ALS10 with the C111Y mutation in the SOD1 gene.