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A mutation in the dynein heavy chain gene compensates for energy deficit of mutant SOD1 mice and increases potentially neuroprotective IGF-1

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by a progressive loss of motor neurons. ALS patients, as well as animal models such as mice overexpressing mutant SOD1s, are characterized by increased energy expenditure. In mice, this hypermetabolism...

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Detalles Bibliográficos
Autores principales: Fergani, Anissa, Eschbach, Judith, Oudart, Hugues, Larmet, Yves, Schwalenstocker, Birgit, Ludolph, Albert C, Loeffler, Jean-Philippe, Dupuis, Luc
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3111394/
https://www.ncbi.nlm.nih.gov/pubmed/21521523
http://dx.doi.org/10.1186/1750-1326-6-26