Creatine supplementation and riluzole treatment provide similar beneficial effects in copper, zinc superoxide dismutase (G93A) transgenic mice

This study investigated the effects of riluzole (Ril), creatine (Cr) and a combination of these treatments on the onset and progression of clinical signs and neuropathology in an animal model of familial amyotrophic lateral sclerosis, the G93A transgenic mouse ( n=13–17 per group). The onset of clin...

Ausführliche Beschreibung

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	Neuroscience 2003-01, Vol.119 (3), p.661-667
Hauptverfasser:	Snow, R.J, Turnbull, J, da Silva, S, Jiang, F, Tarnopolsky, M.A
Format:	Artikel
Sprache:	eng
Schlagworte:	Age of Onset amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - drug therapy Amyotrophic Lateral Sclerosis - enzymology Amyotrophic Lateral Sclerosis - genetics Animals Anterior Horn Cells - drug effects Anterior Horn Cells - enzymology Anterior Horn Cells - pathology Biological and medical sciences Cell Death - drug effects Cell Death - genetics Cerebral Cortex - drug effects Cerebral Cortex - enzymology Cerebral Cortex - physiopathology Creatine - pharmacology Creatine - therapeutic use Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disease Models, Animal Drug Synergism Drug Therapy, Combination Female Male Medical sciences Mice Mice, Transgenic motor neuron disease Muscle, Skeletal - drug effects Muscle, Skeletal - enzymology Neurology Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use nutritional supplement riluzole Riluzole - pharmacology Riluzole - therapeutic use superoxide dismutase Superoxide Dismutase - deficiency Superoxide Dismutase - genetics Treatment Outcome
Online-Zugang:	Volltext
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

Beschreibung
Zusammenfassung:	This study investigated the effects of riluzole (Ril), creatine (Cr) and a combination of these treatments on the onset and progression of clinical signs and neuropathology in an animal model of familial amyotrophic lateral sclerosis, the G93A transgenic mouse ( n=13–17 per group). The onset of clinical signs was delayed ( P
ISSN:	0306-4522 1873-7544
DOI:	10.1016/S0306-4522(03)00212-4