We chose human-SODG93A transgenic mice because a fraction of familial ALS is associated with mutations in the superoxide dismutase gene (SOD1).25 Mouse models expressing ALS-linked human-SOD1 mutations effectively recapitulate many features of the human disease and have been extensively used to investigate pathogenic mechanisms of ALS.26 We performed longitudinal studies on the ENS, microbiome, and SOD1 aggregation in the ALS G93A mice. Here, SOD1 is linked to amyotrophic lateral sclerosis.