GDNF and amyotrophic lateral sclerosis: In this study, we investigated in parallel the expression levels of GDNF and APP and its metabolites in muscles from non-transgenic mice and transgenic mice overexpressing the wild-type human isoform of the Cu/Zn superoxide dismutase 1 (SOD1WT) enzyme or the mutant SOD1G93A protein, the latter animals recapitulating much of the pathophysiology of ALS.