J
Jack P. Antel
Researcher at Montreal Neurological Institute and Hospital
Publications - 540
Citations - 49656
Jack P. Antel is an academic researcher from Montreal Neurological Institute and Hospital. The author has contributed to research in topics: Multiple sclerosis & Microglia. The author has an hindex of 105, co-authored 519 publications receiving 43950 citations. Previous affiliations of Jack P. Antel include Université de Montréal & Howard Hughes Medical Institute.
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Mechanism of γδ T cell-induced human oligodendrocyte cytotoxicity: relevance to multiple sclerosis
TL;DR: Findings suggest that in MS, γδ T cells may utilize either the Fas-mediated or Perforin-based cell cytotoxicity pathways in exerting oligodendrocyte damage, though the Per forin pathway is predominant.
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Dexamethasone suppression test abnormalities in multiple sclerosis: relation to ACTH therapy.
TL;DR: The 1-mg overnight dexamethasone suppression test (DST) in patients with MS may be a useful neuroendocrine test of glucocorticoid sensitivity in MS patients.
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Reduction of the peripheral blood CD56(bright) NK lymphocyte subset in FTY720-treated multiple sclerosis patients.
Trina A. Johnson,Barbara L. Evans,Bryce A. Durafourt,Manon Blain,Yves Lapierre,Amit Bar-Or,Jack P. Antel +6 more
TL;DR: Subset alterations and function of NK cell populations will need to be considered as part of assessing overall immunosurveillance capacity of patients with MS who will receive sustained FTY720 therapy.
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Resistance of human adult oligodendrocytes to AMPA/kainate receptor-mediated glutamate injury
Karolina Wosik,Francesca Ruffini,Guillermina Almazan,André Olivier,Josephine Nalbantoglu,Jack P. Antel +5 more
TL;DR: It is found that human adult OLs in vitro express low levels of ionotropic glutamate receptors and are resistant to excitotoxicity mediated by high and sustained doses of AMPA or kainate, even when receptor desensitization is blocked.
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Origin of contralateral reactive gliosis in surgically injured rat cerebral cortex
TL;DR: The results suggest that the origin of contralateral gliosis in cortical stab injury is more likely due to the release of soluble substance(s) which diffuse to distant areas, rather than the migration of astrocytes through the corpus callosum from the lesion site, or being subsequent to degeneration of neurons which fibers traverse the corpuscallosum.