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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

By Anissa Fergani, Judith Eschbach, Hugues Oudart, Yves Larmet, Birgit Schwalenstocker, Albert C Ludolph, Jean-Philippe Loeffler and Luc Dupuis
Topics: Research Article
Publisher: BioMed Central
OAI identifier: oai:pubmedcentral.nih.gov:3111394
Provided by: PubMed Central

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Citations

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  2. (2004). JP: Evidence for defective energy homeostasis in amyotrophic lateral sclerosis: benefit of a high-energy diet in a transgenic mouse model. Proc Natl Acad Sci USA
  3. (2007). JP: Increased peripheral lipid clearance in an animal model of amyotrophic lateral sclerosis.