On the other hand, similar experiments using a transgenic mouse expressing an NFH β-galactosidase fusion protein, which aggregates and sequesters neurofilaments in neuronal cell bodies, showed no significant alteration of disease pathology in mouse models of dystonia musculorum and SOD-mediated ALS, though there was some prolongation of neuronal survival and some delay of axon loss [56]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.