Some previous studies revealed that either glutamate transporters or glutamate-transport activities were reduced in transgenic mice expressing ALS-associated SOD1 mutants, indicating the involvement of glutamate excitotoxicity in mediating ALS-mutant SOD1 neuronal toxicity (Bruijn et al., 1997; Bendotti et al., 2001; Warita et al., 2002; Boston-Howes et al., 2006; Yamanaka et al., 2008). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.