F
François Gros-Louis
Researcher at Laval University
Publications - 42
Citations - 2690
François Gros-Louis is an academic researcher from Laval University. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Medicine. The author has an hindex of 18, co-authored 34 publications receiving 2408 citations. Previous affiliations of François Gros-Louis include McGill University Health Centre & Centre Hospitalier Universitaire Sainte-Justine.
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Journal ArticleDOI
Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS
Daryl A. Bosco,Gerardo Morfini,Gerardo Morfini,N. Murat Karabacak,Yuyu Song,Yuyu Song,François Gros-Louis,Piera Pasinelli,Holly Goolsby,Benjamin A. Fontaine,Nathan Lemay,Diane McKenna-Yasek,Matthew P. Frosch,Jeffrey N. Agar,Jean-Pierre Julien,Scott T. Brady,Scott T. Brady,Robert H. Brown +17 more
TL;DR: It is suggested that wild-type S OD1 can be pathogenic in SALS and an SOD1-dependent pathogenic mechanism common to FALS and SALS is identified.
Journal ArticleDOI
Mutations in SYNE1 lead to a newly discovered form of autosomal recessive cerebellar ataxia.
François Gros-Louis,Nicolas Dupré,Nicolas Dupré,Patrick A. Dion,Michael A. Fox,Sandra Laurent,Steve Verreault,Joshua R. Sanes,Jean-Pierre Bouchard,Guy A. Rouleau +9 more
TL;DR: It is reported that a newly discovered form of recessive ataxia is found in a French-Canadian cohort and it is shown that SYNE1 mutations are causative in all of the authors' kindreds, making SYne1 the first identified gene responsible for a recessively inherited pure cerebellar ataxias.
Journal ArticleDOI
Genetics of familial and sporadic amyotrophic lateral sclerosis.
TL;DR: The pathways leading to the specific motor neurons degeneration in the presence of SOD1 mutations have not been fully identified and this review provides an overview of the genetics of both familial and sporadic forms of ALS.
Journal ArticleDOI
Neuroprotection through Excitability and mTOR Required in ALS Motoneurons to Delay Disease and Extend Survival
Smita Saxena,Francesco Roselli,Katyayani Singh,Kerstin Leptien,Jean-Pierre Julien,François Gros-Louis,Pico Caroni +6 more
TL;DR: It is shown that in mouse models of familial motoneuron (MN) disease, SOD1 mutants specifically render vulnerable MNs dependent on endogenous neuroprotection signaling involving excitability and mammalian target of rapamycin (mTOR) to counteract clinically important disease progression in ALS.
Journal ArticleDOI
Intracerebroventricular infusion of monoclonal antibody or its derived Fab fragment against misfolded forms of SOD1 mutant delays mortality in a mouse model of ALS
TL;DR: In this paper, a passive immunization approach based on intracerebroventricular infusion in G93A-SOD1 mice of monoclonal antibodies specific to misfolded forms of SOD1 was proposed.