MSTN and amyotrophic lateral sclerosis: Accordingly, genetic inhibition of myostatin function or myostatin blockade by several agents (including myostatin antibodies, myostatin propeptide, follistatin-related proteins, soluble type II myostatin receptor) have been shown to be effective in increasing muscle mass and reducing disease severity in the mdx mouse model of Duchenne muscular dystrophy, in the caveolin 3 deficient model of limb-girdle muscular dystrophy 1C (LGMD1C) and in two rodent models of amyotrophic lateral sclerosis [19, 37-40].