Titre
GDNF slows loss of motoneurons but not axonal degeneration or premature death of pmn/pmn mice.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Sagot, Y.
Auteure/Auteur
Tan, S.A.
Auteure/Auteur
Hammang, J.P.
Auteure/Auteur
Aebischer, P.
Auteure/Auteur
Kato, A.C.
Auteure/Auteur
Liens vers les unités
ISSN
0270-6474
Statut éditorial
Publié
Date de publication
1996
Volume
16
Numéro
7
Première page
2335
Dernière page/numéro d’article
2341
Langue
anglais
Résumé
Glial cell line-derived neurotrophic factor (GDNF), a member of the TG F-beta superfamily, has been shown to be a highly potent neurotrophic factor that enhances survival of various neuronal cell types including motoneurons. To assess its therapeutic potential in treating neurodegenerative diseases such as amyotrophic lateral sclerosis, we treated mutant mice displaying motoneuron degeneration (progressive motor neuropathy; pmn) with encapsulated GDNF-secreting cells. Effects of GDNF treatment on pmn/pmn mice were compared with previous results obtained with ciliary neurotrophic factor (CNTF) [Sagot Y, Tan SA, Baetge E, Schmalbruch H, Kato AC, Aebischer P (1995) Eur J Neurosci 7:1313-1322]. In contrast to CNTF, GDNF did not increase the lifespan of pmn/pmn mice. However, GDNF significantly reduced the loss of facial motoneurons by 50%, a value similar to what was observed when CNTF was administered to the pmn/pmn mice. Surprisingly, myelinated axon counts revealed that GDNF had no effect on nerve degeneration. Therefore, despite its potential in rescuing motoneuron cell bodies, the inability of GDNF to prevent nerve degeneration in pmn/pmn mice suggests that its usefulness in the treatment of motor neuron diseases may be restricted to cotreatment with other factors that act on the nerve process.
Sujets
PID Serval
serval:BIB_5894
PMID
Date de création
2007-11-19T11:42:50.903Z
Date de création dans IRIS
2025-05-20T16:10:30Z