Attempts to delineate early changes in ALS, as opposed to those at end-stages, have focused on biopsy material from ALS patients and controls, as well as studies in widely used animal models of ALS such as transgenic rodents over-expressing human mutant SOD (mSOD), which manifest motoneuron degeneration similar to that seen in ALS patients (Turner and Talbot, 2008). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.