| First Author | Petri S | Year | 2006 |
| Journal | J Neurol Sci | Volume | 251 |
| Issue | 1-2 | Pages | 44-9 |
| PubMed ID | 17049562 | Mgi Jnum | J:129276 |
| Mgi Id | MGI:3768968 | Doi | 10.1016/j.jns.2006.08.013 |
| Citation | Petri S, et al. (2006) Loss of Fas ligand-function improves survival in G93A-transgenic ALS mice. J Neurol Sci 251(1-2):44-9 |
| abstractText | ALS is a devastating neurodegenerative disorder for which no effective treatment exists. The precise molecular mechanisms underlying the selective degeneration of motor neurons are still unknown. A motor neuron specific apoptotic pathway involving Fas and NO has been discovered. Motor neurons from ALS-mice have an increased sensitivity to Fas-induced cell death via this pathway. In this study we therefore crossed G93A-SOD1 overexpressing ALS mice with Fas ligand (FasL) mutant (gld) mice to investigate whether the reduced Fas signaling could have beneficial effects on motor neuron death. G93A-SOD1 mutant mice with a homozygous FasL mutant showed a modest but statistically significant extension of survival, and reduced loss of motor neurons. These results indicate that motor neuron apoptosis triggered by Fas is relevant in ALS pathogenesis. |
