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Shifting imaging targets in multiple sclerosis: From inflammation to neurodegeneration
Author(s) -
Vigeveno René M.,
Wiebenga Oliver T.,
Wattjes Mike P.,
Geurts Jeroen J.G.,
Barkhof Frederik
Publication year - 2012
Publication title -
journal of magnetic resonance imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.563
H-Index - 160
eISSN - 1522-2586
pISSN - 1053-1807
DOI - 10.1002/jmri.23578
Subject(s) - multiple sclerosis , medicine , neurodegeneration , disease , neuroprotection , white matter , remyelination , neuroscience , clinical trial , pathological , immune modulation , inflammation , glatiramer acetate , immune system , magnetic resonance imaging , pathology , psychology , central nervous system , immunology , radiology , myelin
Classically multiple sclerosis (MS) has been regarded as an auto‐immune disease of the white matter in the central nervous system leading to severe disability over the course of several decades. Current therapeutic strategies in MS are mostly based on either immune suppression or immune modulation. Although effective in decreasing relapse frequency and severity as well as delaying disease progression, MS pathology ensues nonetheless. In the last decade it became evident that gray matter pathology plays an important role in disease progression and helps explaining certain aspects of MS‐related disability such as cognitive decline. Conventional MRI outcome measures commonly used in clinical trials are sufficient to demonstrate an anti‐inflammatory drug‐effect but lack pathological specificity and are poor to moderate predictors of disability. In this article, we review new insights in gray matter pathology and functional reorganization in MS and how these novel fields in MS research may validate and establish new MRI outcome measures, aid in the development of new therapeutic strategies for neuroprotection and neurorepair, and may lead to development of novel predictive measures of disability and disease progression in MS. J. Magn. Reson. Imaging 2012; 36:1–19. © 2012 Wiley Periodicals, Inc.

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