Repurposing of Trimetazidine for Amyotrophic Lateral Sclerosis: a study in SOD1 mice.
Fiche publication
Date publication
novembre 2021
Journal
British journal of pharmacology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr LOEFFLER Jean-Philippe
Tous les auteurs :
Scaricamazza S, Salvatori I, Amadio S, Nesci V, Torcinaro A, Giacovazzo G, Primiano A, Gloriani M, Candelise N, Pieroni L, Loeffler JP, Renè F, Quessada C, Tefera TW, Wang H, Steyn FJ, Ngo ST, Dobrowolny G, Lepore E, Urbani A, Musarò A, Volonté C, Ferraro E, Coccurello R, Valle C, Ferri A
Lien Pubmed
Résumé
Amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characterized by the degeneration of upper and lower motor neurons, progressive wasting and paralysis of voluntary muscles is currently incurable despite intense research and numerous unsuccessful clinical trials. Although considered as a pure motor neuron disease, increasing evidence indicates that the sole protection of motor neurons by a single target drug is not sufficient to improve the pathological phenotype. We therefore evaluated the therapeutic potential of the multi-target drug, trimetazidine, in SOD1 mice.
Mots clés
Amyotrophic Lateral Sclerosis, Hypermetabolism, Mitochondria, Neurodegeneration, SOD1G93A mice, Trimetazidine
Référence
Br J Pharmacol. 2021 Nov 16;: