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  • Title: Loss of Fas ligand-function improves survival in G93A-transgenic ALS mice.
    Author: Petri S, Kiaei M, Wille E, Calingasan NY, Flint Beal M.
    Journal: J Neurol Sci; 2006 Dec 21; 251(1-2):44-9. PubMed ID: 17049562.
    Abstract:
    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.
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