The transgenic superoxide dismutase 1 (mSOD1) ALS mouse model, which partially recapitulates the phenotype of human ALS, has shown increased type I (secreted) NRG1 expression that could contribute to disease progression as it was associated with glial cell activation (though type III (membrane-bound) NRG1 expression was reduced in parallel with motor neuron loss) [40]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.