G
Guy A. Rouleau
Researcher at Montreal Neurological Institute and Hospital
Publications - 935
Citations - 75050
Guy A. Rouleau is an academic researcher from Montreal Neurological Institute and Hospital. The author has contributed to research in topics: Gene & Genome-wide association study. The author has an hindex of 129, co-authored 884 publications receiving 65892 citations. Previous affiliations of Guy A. Rouleau include Utrecht University & University of Helsinki.
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Models for inherited susceptibility to cancer in the nervous system: a molecular-genetic approach to neurofibromatosis.
TL;DR: Different molecular-genetic approaches towards identifying and characterization of the NF genes, based on their chromosomal localizations, will have profound implications for diagnosis and treatment of these diseases and might yield significant insights into mechanisms controlling development and differentiation of the human nervous system.
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Clinical features associated with an early onset in chronic tic disorders.
Francois Richer,Francois Richer,Roula Daghfal,Guy A. Rouleau,Paul Lespérance,Sylvain Chouinard +5 more
TL;DR: The results suggest that an early onset affects symptom expression in tic disorders, and tics often appear in early childhood, a period in which symptom expression may be affected by early brain development.
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Purification of the NF2 Tumor Suppressor Protein from Human Erythrocytes
Hitesh K. Jindal,Kazumi Yoshinaga,Pil-Soo Seo,Mohini Lutchman,Patrick A. Dion,Guy A. Rouleau,Toshihiko Hanada,Athar H. Chishti +7 more
TL;DR: Evidence is provided for the presence of NF2 protein in the human erythrocyte membrane that is distinct from the known membrane interactions of protein 4.1, which is an autosomal dominant disease predisposing individuals to the risk of developing tumors of cranial and spinal nerves.
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A founder mutation in French-Canadian families with X-linked hereditary neuropathy.
Nicolas Dupré,Louise Cossette,Collette K. Hand,Jean-Pierre Bouchard,Guy A. Rouleau,Jack Puymirat +5 more
TL;DR: The study suggests that the Ser26Trp mutation may cause a primary demyelinating neuropathy that is not associated with a specific clinical phenotype and finds evidence that the majority of kindreds share a common ancestor.
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No effect on SOD1 splicing by TARDP or FUS mutations
TL;DR: The aim was to assess if TARDBP and/or FUS ALS-predisposing mutations that are known to lead to the accumulation of TDP-43 or FUS aggregations in the cytoplasm also lead to aberrant S OD1 RNA splicing events, and to determine if SOD1 could be an RNA target for TDP -43, FUS, or both.