This suggests that elevated levels of D-serine contribute to motor neuron degeneration which is supported by the findings concerning two mutations in DAO that virtually abolish enzyme activity, one that is associated in familial ALS in man and a second found in the mouse that causes a motor phenotype similar to that seen in the SOD1 mouse model of ALS (Sasabe et al., 2012). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.