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      Possible regenerative effects of fingolimod (FTY720) in multiple sclerosis disease: An overview on remyelination process

      1 , 2 , 3 , 4 , 5
      Journal of Neuroscience Research
      Wiley

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          Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination.

          Multiple sclerosis (MS) is a disease with profound heterogeneity in clinical course, neuroradiological appearance of the lesions, involvement of susceptibility gene loci, and response to therapy. These features are supported by experimental evidence, which demonstrates that fundamentally different processes, such as autoimmunity or virus infection, may induce MS-like inflammatory demyelinating plaques and suggest that MS may be a disease with heterogeneous pathogenetic mechanisms. From a large pathology sample of MS, collected in three international centers, we selected 51 biopsies and 32 autopsies that contained actively demyelinating lesions defined by stringent criteria. The pathology of the lesions was analyzed using a broad spectrum of immunological and neurobiological markers. Four fundamentally different patterns of demyelination were found, defined on the basis of myelin protein loss, the geography and extension of plaques, the patterns of oligodendrocyte destruction, and the immunopathological evidence of complement activation. Two patterns (I and II) showed close similarities to T-cell-mediated or T-cell plus antibody-mediated autoimmune encephalomyelitis, respectively. The other patterns (III and IV) were highly suggestive of a primary oligodendrocyte dystrophy, reminiscent of virus- or toxin-induced demyelination rather than autoimmunity. At a given time point of the disease--as reflected in autopsy cases--the patterns of demyelination were heterogeneous between patients, but were homogenous within multiple active lesions from the same patient. This pathogenetic heterogeneity of plaques from different MS patients may have fundamental implications for the diagnosis and therapy of this disease.
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            Multiple sclerosis review.

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              A mechanistically novel, first oral therapy for multiple sclerosis: the development of fingolimod (FTY720, Gilenya).

              Multiple sclerosis (MS) is a chronic autoimmune disorder affecting the central nervous system (CNS) through demyelination and neurodegeneration. Until recently, major therapeutic treatments have relied on agents requiring injection delivery. In September 2010, fingolimod/FTY720 (Gilenya, Novartis) was approved by the FDA as the first oral treatment for relapsing forms of MS. Fingolimod is a novel compound produced by chemical modification of a fungal precursor. Its active metabolite, formed by in vivo phosphorylation, modulates sphingosine 1-phosphate (S1P) receptors that are a subset of a larger family of cell-surface, G protein-coupled receptors (GPCRs) mediating the effects of bioactive lipids known as lysophospholipids. Fingolimod's mechanism of action in MS is not completely understood; however, its relevant biology indicates a fundamentally different mechanism compared to all previously approved MS therapies, with evolving research supporting both immunological and nervous system activities. This duality may herald a paradigm shift in the treatment of MS and other neurological disorders.
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                Author and article information

                Contributors
                Journal
                Journal of Neuroscience Research
                J Neurosci Res
                Wiley
                0360-4012
                1097-4547
                March 2020
                August 05 2019
                March 2020
                : 98
                : 3
                : 524-536
                Affiliations
                [1 ]Department of Physiology, School of Medicine Isfahan University of Medical Sciences Isfahan Iran
                [2 ]Cellular and Molecular Biology Research Center Health Research Institute, Babol University of Medical Sciences Babol Iran
                [3 ]Neuroscience Research Center Health Research Institute, Babol University of Medical Sciences Babol Iran
                [4 ]Department of Physiology, Faculty of Medical Sciences Tarbiat Modares University Tehran Iran
                [5 ]Department of Brain and Cognitive Sciences, Cell Science Research Center Royan Institute for Stem Cell Biology and Technology, ACECR Tehran Iran
                Article
                10.1002/jnr.24509
                31385341
                037dca62-8c33-49e0-bb4a-1a278abeca81
                © 2020

                http://onlinelibrary.wiley.com/termsAndConditions#vor

                http://doi.wiley.com/10.1002/tdm_license_1.1

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