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Pathology and disease mechanisms in different stages of multiple sclerosis

Lassmann, Hans·2013·Journal of the Neurological Sciences
DOI 10.1016/j.jns.2013.05.010
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Abstract

In this review the differences in pathology and disease mechanisms between early and late stages of multiple sclerosis are discussed. The data suggest that affection of the brain is different, depending on the location of lesions, on the stage of the disease, when lesions arise, and on inter-individual differences between patients. We suggest that in the early stage of the disease new lesions are formed by new waves of inflammatory cells, entering the central nervous system from the circulation and giving rise to focal demyelinated plaques in the white and gray matter. In contrast, at late stages of the disease inflammation decreases, but the susceptibility of the target tissue for neurodegeneration increases. New data suggest that mitochondrial injury, mediated through oxidative injury, is in the center of the pathogenetic events leading to brain damage in multiple sclerosis patients.

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  1. Babbe, 2000, Clonal expansion of CD8+ T cells dominate the T cell infiltrate in active multiple sclerosis lesions as shown by micromanipulation and single cell polymerase chain reaction, J Exp Med, 192, 393, 10.1084/jem.192.3.393 · DOI · Paper page
  2. Esiri, 1980, Multiple sclerosis: A quantitative and qualitative study of immunoglobulin-containing cells in the central nervous system, Neuropathol Appl Neurobiol, 6, 9, 10.1111/j.1365-2990.1980.tb00199.x · DOI
  3. Frischer, 2009, The relation between inflammation and neurodegeneration in multiple sclerosis, Brain, 132, 1175, 10.1093/brain/awp070 · DOI · Paper page
  4. Hoftberger, 2004, Expression of major histocompatibility complex class I molecules on the different cell types in multiple sclerosis lesions, Brain Pathol, 14, 43, 10.1111/j.1750-3639.2004.tb00496.x · DOI
  5. Holman, 1812, The blood brain barrier, chemokines and multiple sclerosis, Biochim Biophys Acta, 2011, 220
  6. Bjartmar, 2000, Neurological disability correlates with spinal cord axonal loss and reduced N-acetyl aspartate in chronic multiple sclerosis patients, Ann Neurol, 48, 893, 10.1002/1531-8249(200012)48:6<893::AID-ANA10>3.0.CO;2-B · DOI
  7. Kutzelnigg, 2005, Cortical demyelination and diffuse white matter injury in multiple sclerosis, Brain, 128, 2705, 10.1093/brain/awh641 · DOI · Paper page
  8. Cifelli, 2002, Thalamic neurodegeneration in multiple sclerosis, Ann Neurol, 52, 650, 10.1002/ana.10326 · DOI
  9. Gilmore, 2009, Spinal cord grey matter lesions in multiple sclerosis detected by post-mortem high field MR imaging, Mult Scler, 15, 180, 10.1177/1352458508096876 · DOI
  10. Patrikios, 2006, Remyelination is extensive in a subset of multiple sclerosis patients, Brain, 129, 3165, 10.1093/brain/awl217 · DOI · Paper page
  11. Albert, 2007, Extensive cortical remyelination in patients with chronic multiple sclerosis, Brain Pathol, 17, 129, 10.1111/j.1750-3639.2006.00043.x · DOI · Paper page
  12. Kornek, 2000, Multiple sclerosis and chronic autoimmune encephalomyelitis: a comparative quantitative study of axonal injury in active, inactive and remyelinated lesions, Amer J Pathol, 157, 267, 10.1016/S0002-9440(10)64537-3 · DOI
  13. Prineas, 1993, Multiple sclerosis. Pathology of recurrent lesions, Brain, 116, 681, 10.1093/brain/116.3.681 · DOI
  14. Bramow, 2010, Demyelination versus remyelination in progressive multiple sclerosis, Brain, 133, 2983, 10.1093/brain/awq250 · DOI
  15. Lublin, 1996, Defining the clinical course of multiple sclerosis: results of an international survey. National Multiple Sclerosis Society (USA) Advisory Committee on Clinical Trials of New Agents in Multiple Sclerosis, Neurology, 46, 907, 10.1212/WNL.46.4.907 · DOI
  16. Wiendl, 2009, Multiple sclerosis therapeutics: unexpected outcomes clouding undisputed successes, Neurology, 72, 1008, 10.1212/01.wnl.0000344417.42972.54 · DOI
  17. Giacomini, 2009, Emerging multiple sclerosis disease-modifying therapies, Curr Opin Neurol, 22, 226, 10.1097/WCO.0b013e32832b4ca1 · DOI
  18. Magliozzi, 2010, A gradient of neuronal loss and meningeal inflammation in multiple sclerosis, Ann Neurol, 68, 477, 10.1002/ana.22230 · DOI · Paper page
  19. Magliozzi, 2007, Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology, Brain, 130, 1089, 10.1093/brain/awm038 · DOI
  20. Hochmeister, 2006, Dysferlin is a new marker for leaky brain blood vessels in multiple sclerosis, J Neuropathol Exp Neurol, 65, 855, 10.1097/01.jnen.0000235119.52311.16 · DOI · Paper page
  21. Serafini, 2004, Detection of ectopic B-cell follicles with germinal centers in the meninges of patients with secondary progressive multiple sclerosis, Brain Pathol, 14, 164, 10.1111/j.1750-3639.2004.tb00049.x · DOI · Paper page
  22. Howell, 2011, Meningeal inflammation is widespread and linked to cortical pathology in multiple sclerosis, Brain, 134, 2755, 10.1093/brain/awr182 · DOI · Paper page
  23. Ozawa, 1994, Patterns of oligodendroglia pathology in multiple sclerosis, Brain, 117, 1311, 10.1093/brain/117.6.1311 · DOI
  24. Brück, 1995, Monocyte/macrophage differentiation in early multiple sclerosis, Ann Neurol, 38, 788, 10.1002/ana.410380514 · DOI
  25. Prineas, 2001, Immunopathology of secondary-progressive multiple sclerosis, Ann Neurol, 50, 646, 10.1002/ana.1255 · DOI
  26. Bo, 2003, Subpial demyelination in the cerebral cortex of multiple sclerosis patients, J Neuropathol Exp Neurol, 62, 723, 10.1093/jnen/62.7.723 · DOI · Paper page
  27. Moll, 2008, Cortical demyelination in PML and MS: similarities and differences, Neurology, 70, 336, 10.1212/01.wnl.0000284601.54436.e4 · DOI
  28. Kolasinski, 2012, A combined post-mortem MRI and quantitative histological study of multiple sclerosis pathology, Brain, 135, 2938, 10.1093/brain/aws242 · DOI
  29. Lassmann, 2012, Cortical lesions in multiple sclerosis: inflammation versus neurodegeneration, Brain, 135, 2904, 10.1093/brain/aws260 · DOI
  30. Evangelou, 2000, Regional axonal loss in the corpus callosum correlates with cerebral white matter lesion volume and distribution in multiple sclerosis, Brain, 123, 1845, 10.1093/brain/123.9.1845 · DOI
  31. DeLuca, 2006, The contribution of demyelination to axonal loss in multiple sclerosis, Brain, 129, 1507, 10.1093/brain/awl074 · DOI
  32. Wegner, 2006, Neocortical neuronal, synaptic, and glial loss in multiple sclerosis, Neurology, 67, 960, 10.1212/01.wnl.0000237551.26858.39 · DOI
  33. Lucchinetti, 2000, Heterogeneity of multiple sclerosis lesions: Implications for the pathogenesis of demyelination, Ann Neurol, 47, 707, 10.1002/1531-8249(200006)47:6<707::AID-ANA3>3.0.CO;2-Q · DOI
  34. Lassmann, 2011, The molecular basis of neurodegeneration in multiple sclerosis, FEBS Lett, 585, 3715, 10.1016/j.febslet.2011.08.004 · DOI
  35. Mahad, 2008, Mitochondrial defects in acute multiple sclerosis lesions, Brain, 131, 1722, 10.1093/brain/awn105 · DOI · Paper page
  36. Cross, 1998, Peroxynitrite formation within the central nervous system in active multiple sclerosis, J Neuroimmunol, 88, 45, 10.1016/S0165-5728(98)00078-2 · DOI
  37. Liu, 2001, Expression of indicible nitric oxide synthase and nitrotyrosine in multiple sclerosis lesions, Amer J Pathol, 158, 2057, 10.1016/S0002-9440(10)64677-9 · DOI
  38. Fischer, 2012, NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury, Brain, 135, 886, 10.1093/brain/aws012 · DOI · Paper page
  39. Marik, 2007, Lesion genesis in a subset of patients with multiple sclerosis: a role for innate immunity?, Brain, 130, 2800, 10.1093/brain/awm236 · DOI · Paper page
  40. Gray, 2008, Elevated myeloperoxidase activity in white matter in multiple sclerosis, Neurosci Lett, 442, 195, 10.1016/j.neulet.2008.08.035 · DOI
  41. Haider, 2011, Oxidative damage and neurodegeneration in multiple sclerosis lesions, Brain, 134, 1914, 10.1093/brain/awr128 · DOI
  42. Hallgren, 1958, The effect of age on the non-haemin iron in the human brain, J Neurochem, 3, 41, 10.1111/j.1471-4159.1958.tb12607.x · DOI · Paper page
  43. Hulet, 1999, Distribution of transferrin and ferritin binding in normal and multiple sclerotic human brain, J Neurol Sci, 165, 48, 10.1016/S0022-510X(99)00077-5 · DOI
  44. Campbell, 2011, Mitochondrial DNA deletions and neurodegeneration in multiple sclerosis, Ann Neurol, 69, 481, 10.1002/ana.22109 · DOI

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Metadata

Authors
Lassmann, H.
Venue
Journal of the Neurological Sciences
Publisher
Elsevier BV
Published
2013-10
Volume
333
Issue
1-2
Pages
1-4
ISSN
0022-510X
DOI
10.1016/j.jns.2013.05.010
Cited by
224
References
6
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Funders
Austrian Science Fund (24245)

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