SOD1 and Motor neuron atrophy: Indeed, SOD1 in other species can also aggregate without tryptophan; for example, despite dogs and mice lacking W32, and having major sequence divergence at sequence segment 28–38 (canine = 64% identity, mouse = 55% identity) (Supplementary Fig. 10), dogs can develop canine degenerative myelopathy with SOD1 mutations48, while transgenic mice carrying a G86R mutation in murine SOD1 develop disease that features motor neuron degeneration and SOD1 positive inclusions49,50.