| First Author | Rose FF Jr | Year | 2008 |
| Journal | Biochem Biophys Res Commun | Volume | 375 |
| Issue | 1 | Pages | 119-23 |
| PubMed ID | 18680723 | Mgi Jnum | J:140130 |
| Mgi Id | MGI:3811970 | Doi | 10.1016/j.bbrc.2008.07.130 |
| Citation | Rose FF Jr, et al. (2008) The Wallerian degeneration slow (Wld(s)) gene does not attenuate disease in a mouse model of spinal muscular atrophy. Biochem Biophys Res Commun 375(1):119-23 |
| abstractText | Spinal muscular atrophy (SMA) is a severe neuromuscular disease characterized by loss of spinal alpha-motor neurons, resulting in the paralysis of skeletal muscle. SMA is caused by deficiency of survival motor neuron (SMN) protein levels. Recent evidence has highlighted an axon-specific role for SMN protein, raising the possibility that axon degeneration may be an early event in SMA pathogenesis. The Wallerian degeneration slow (Wld(s)) gene is a spontaneous dominant mutation in mice that delays axon degeneration by approximately 2-3 weeks. We set out to examine the effect of Wld(s) on the phenotype of a mouse model of SMA. We found that Wld(s) does not alter the SMA phenotype, indicating that Wallerian degeneration does not directly contribute to the pathogenesis of SMA development. |
