Literature DB >> 15177777

The pathogenesis and basis for treatment in multiple sclerosis.

Alastair Compston1.   

Abstract

The central concept underlying ideas on the pathogenesis of multiple sclerosis is that inflammatory events cause acute injury of axons and myelin. The phases of symptom onset, recovery, persistence and progression in multiple sclerosis can be summarized as functional impairment with intact structure due to direct effects of inflammatory mediators, demyelination and axonal injury with recovery through plasticity and remyelination, and chronic axonal loss due to failure of enduring remyelination from loss of trophic support for axons normally provided by cells of the oligodendrocyte lineage.

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Year:  2004        PMID: 15177777     DOI: 10.1016/j.clineuro.2004.02.007

Source DB:  PubMed          Journal:  Clin Neurol Neurosurg        ISSN: 0303-8467            Impact factor:   1.876


  12 in total

1.  T-cell-mediated disruption of the neuronal microtubule network: correlation with early reversible axonal dysfunction in acute experimental autoimmune encephalomyelitis.

Authors:  Leah P Shriver; Bonnie N Dittel
Journal:  Am J Pathol       Date:  2006-09       Impact factor: 4.307

2.  Conditional Tet-regulated over-expression of Hoxa2 in CG4 cells increases their proliferation and delays their differentiation into oligodendrocyte-like cells expressing myelin basic protein.

Authors:  Monica Wang; J Ronald Doucette; Adil J Nazarali
Journal:  Cell Mol Neurobiol       Date:  2011-04-09       Impact factor: 5.046

3.  Immunopathogenesis of multiple sclerosis.

Authors:  Michael K Racke
Journal:  Ann Indian Acad Neurol       Date:  2009-10       Impact factor: 1.383

Review 4.  Complement in multiple sclerosis: its role in disease and potential as a biomarker.

Authors:  G Ingram; S Hakobyan; N P Robertson; B P Morgan
Journal:  Clin Exp Immunol       Date:  2008-11-24       Impact factor: 4.330

5.  CD8+ T cells directed against a viral peptide contribute to loss of motor function by disrupting axonal transport in a viral model of fulminant demyelination.

Authors:  Charles L Howe; Daren Ure; Jaimie D Adelson; Reghann LaFrance-Corey; Aaron Johnson; Moses Rodriguez
Journal:  J Neuroimmunol       Date:  2007-05-09       Impact factor: 3.478

Review 6.  Calpain-mediated signaling mechanisms in neuronal injury and neurodegeneration.

Authors:  P S Vosler; C S Brennan; J Chen
Journal:  Mol Neurobiol       Date:  2008-08-07       Impact factor: 5.590

Review 7.  Toll-like receptors in multiple sclerosis.

Authors:  Michael K Racke; Paul D Drew
Journal:  Curr Top Microbiol Immunol       Date:  2009       Impact factor: 4.291

Review 8.  Inflammasome Signaling in the Aging Brain and Age-Related Neurodegenerative Diseases.

Authors:  Subhashini Brahadeeswaran; Narmadhaa Sivagurunathan; Latchoumycandane Calivarathan
Journal:  Mol Neurobiol       Date:  2022-01-23       Impact factor: 5.590

9.  Enhanced disease reduction using clozapine, an atypical antipsychotic agent, and glatiramer acetate combination therapy in experimental autoimmune encephalomyelitis.

Authors:  Laura K Green; Pirooz Zareie; Nikki Templeton; Robert A Keyzers; Bronwen Connor; Anne Camille La Flamme
Journal:  Mult Scler J Exp Transl Clin       Date:  2017-03-17

10.  Myeloid cell transmigration across the CNS vasculature triggers IL-1β-driven neuroinflammation during autoimmune encephalomyelitis in mice.

Authors:  Sébastien A Lévesque; Alexandre Paré; Benoit Mailhot; Victor Bellver-Landete; Hania Kébir; Marc-André Lécuyer; Jorge Ivan Alvarez; Alexandre Prat; Juan Pablo de Rivero Vaccari; Robert W Keane; Steve Lacroix
Journal:  J Exp Med       Date:  2016-05-02       Impact factor: 14.307

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