Furthermore, mutant SOD1 in microglia and astrocytes enhanced nitrogen oxides oxidation resulting in reactive oxygen species production, and treatment with a nitrogen oxides inhibitor not only attenuated glial cell toxicity, but also increased significantly the life span of ALS mice.9 Thus, a therapeutic strategy delivering effective antioxidants could provide significant protection of motor neurons in ALS. Here, SOD1 is linked to amyotrophic lateral sclerosis.