Cortical pathology in multiple sclerosis: experimental approaches to studies on the mechanisms of demyelination and remyelination

2012 ◽  
Vol 126 ◽  
pp. 97-102 ◽  
Author(s):  
S. M. Staugaitis ◽  
A. Chang ◽  
B. D. Trapp
Keyword(s):  
Multiple Sclerosis ◽  
Experimental Approaches ◽  
Cortical Pathology

scholarly journals Cortical pathology in multiple sclerosis detected by the T1/T2-weighted ratio from routine magnetic resonance imaging

2017 ◽  
Vol 82 (4) ◽  
pp. 519-529 ◽  
Author(s):  
Ruthger Righart ◽  
Viola Biberacher ◽  
Laura E. Jonkman ◽  
Roel Klaver ◽  
Paul Schmidt ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Multiple Sclerosis ◽  
Magnetic Resonance ◽  
Resonance Imaging ◽  
Routine Magnetic Resonance Imaging ◽  
Cortical Pathology

Cortical pathology in multiple sclerosis

2008 ◽  
Vol 21 (3) ◽  
pp. 229-234 ◽  
Author(s):  
Christine Stadelmann ◽  
Monika Albert ◽  
Christiane Wegner ◽  
Wolfgang Brück
Keyword(s):  
Multiple Sclerosis ◽  
Cortical Pathology

scholarly journals 7 Tesla Magnetic Resonance Imaging to Detect Cortical Pathology in Multiple Sclerosis

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e108863 ◽  
Author(s):  
Bing Yao ◽  
Simon Hametner ◽  
Peter van Gelderen ◽  
Hellmuth Merkle ◽  
Christina Chen ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Multiple Sclerosis ◽  
Magnetic Resonance ◽  
7 Tesla ◽  
Resonance Imaging ◽  
Cortical Pathology

To what extent is oligodendrocyte progenitor migration a limiting factor in the remyelination of multiple sclerosis lesions?

1997 ◽  
Vol 3 (2) ◽  
pp. 84-87 ◽  
Author(s):  
Robin JM Franklin ◽  
William F Blakemore
Keyword(s):  
Multiple Sclerosis ◽  
Glial Cell ◽  
Cell Transplantation ◽  
Limiting Factor ◽  
Limited Area ◽  
Long Distance ◽  
Oligodendrocyte Progenitor ◽  
Demyelinating Lesions ◽  
X Irradiation ◽  
Experimental Approaches

In this article we describe a series of experimental approaches, involving the use of gliotoxin-induced demyelination, X-irradiation and glial cell transplantation, which examine the size of the area around demyelinating lesions from which new remyelinating cells are generated, and the distance over which they are able to migrate. Taken together, these studies suggest that the recruitment of remyelinating cells takes place over a very limited area and that long distance migration of remyelinating cells is not a feature of remyelination. The implications of these findings for spontaneous remyelination of multiple sclerosis plaques, and the development of strategies for enhancing remyelination are discussed.

Natalizumab strongly suppresses cortical pathology in relapsing–remitting multiple sclerosis

2012 ◽  
Vol 18 (12) ◽  
pp. 1760-1767 ◽  
Author(s):  
F Rinaldi ◽  
M Calabrese ◽  
D Seppi ◽  
M Puthenparampil ◽  
P Perini ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Reference Population ◽  
Cortical Atrophy ◽  
Cortical Lesion ◽  
Cognitive Disability ◽  
Cortical Lesions ◽  
Immunomodulatory Agents ◽  
Relapsing Remitting ◽  
Relevant Role ◽  
Cortical Pathology

Background: Since cortical pathology has been indicated to play a relevant role in the physical and cognitive disability of multiple sclerosis (MS) patients, this study aims to analyze the efficacy of natalizumab in slowing down its progression. Methods: A total of 120 relapsing–remitting MS patients completed a 2-year prospective study: 35 received natalizumab, 50 received interferon beta-1a or glatiramer acetate (immunomodulatory agents - IMA) and 35 remained untreated. Forty healthy subjects constituted the reference population. Clinical and magnetic resonance imaging (MRI) evaluations (including cortical lesions and atrophy) were performed at baseline and after 2 years. Results: Natalizumab significantly reduced accumulation of new cortical lesions (0.2±0.6,range 0–3) compared to immunomodulatory agents (1.3±1.1 togli spazio, range 1–6, p=0.001) and no treatment (2.9±1.5, range 1–8, p<0.001). The percentage of patients with new cortical lesions was also lower in natalizumab-treated patients (20%) compared to IMA-treated and untreated patients (68.0% and 74.2%; p<0.001 for both comparisons). Furthermore, the progression of cortical atrophy was significantly reduced by natalizumab (% change=1.7%) compared to IMA (3.7%, p=0.003) and no therapy (4.6%, p<0.001). Finally, a greater percentage (51.4%) of natalizumab-treated patients remained disease-free (no clinical or MRI evidence of disease activity or progression) compared to IMA-treated (18%, p=0.001) and untreated patients (5.7%, p<0.001). Conclusions: Natalizumab treatment significantly decreases cortical lesion accumulation and cortical atrophy progression in severe relapsing–remitting MS. While supporting the inflammatory origin of cortical lesions, our results highlight the significant impact of natalizumab on cortical pathology.

scholarly journals Meningeal inflammation in multiple sclerosis induces phenotypic changes in cortical microglia that differentially associate with neurodegeneration

2020 ◽  
Author(s):  
Lynn van Olst ◽  
Carla Rodriguez-Mogeda ◽  
Carmen Picon-Munoz ◽  
Svenja Kiljan ◽  
Rachel E. James ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Neuronal Loss ◽  
Post Mortem ◽  
Protective Properties ◽  
Phenotypic Changes ◽  
Extensive Analysis ◽  
Meningeal Inflammation ◽  
Cortical Pathology ◽  
Over Time

AbstractMeningeal inflammation strongly associates with demyelination and neuronal loss in the underlying cortex of progressive MS patients, contributing to clinical disability. However, the pathological mechanisms of meningeal inflammation-induced cortical pathology are still largely elusive. Using extensive analysis of human post-mortem tissue, we identified two distinct microglial phenotypes, termed MS1 and MS2, in the cortex of progressive MS patients. These phenotypes differed in morphology and protein expression, but both associated with inflammation of the overlying meninges. We could replicate the MS-specific microglial phenotypes in a novel in vivo rat model for progressive MS-like meningeal inflammation, with microglia present at 1 month post-induction resembling MS1 microglia whereas those at 2 months acquired an MS2-like phenotype. Interestingly, MS1 microglia were involved in presynaptic displacement and phagocytosis and associated with a relative sparing of neurons in the MS and animal cortex. In contrast, the presence of MS2 microglia coincided with substantial neuronal loss. Taken together, we uncovered that in response to meningeal inflammation, microglia acquire two distinct phenotypes that differentially associate with neurodegeneration in the progressive MS cortex. Our data suggests that these phenotypes occur sequentially and that microglia may lose their protective properties over time, contributing to neuronal loss.

Unraveling cortical pathology in multiple sclerosis using the T1-/T2-weighted ratio?

2017 ◽  
Vol 82 (4) ◽  
pp. 516-518
Author(s):  
Caterina Mainero ◽  
Céline Louapre
Keyword(s):  
Multiple Sclerosis ◽  
Cortical Pathology
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