Imperial College London
Alternate

Professor Richard Reynolds, BSc AKC PhD

Faculty of Medicine, Department of Brain Sciences

Professor of Cellular Neurobiology
 
 
 
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Contact

 

+44 (0)20 7594 6668r.reynolds

 
 
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Location

 

E414Burlington DanesHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Bevan:2018:10.1002/ana.25365,
author = {Bevan, RJ and Evans, R and Griffiths, L and Watkins, LM and Rees, MI and Magliozzi, R and Allen, I and McDonnell, G and Kee, R and Naughton, M and Fitzgerald, DC and Reynolds, R and Neal, JW and Howell, OW},
doi = {10.1002/ana.25365},
journal = {Annals of Neurology},
pages = {829--842},
title = {Meningeal inflammation and cortical demyelination in acute multiple sclerosis},
url = {http://dx.doi.org/10.1002/ana.25365},
volume = {84},
year = {2018}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - ObjectiveCortical gray matter (GM) pathology, involving demyelination and neurodegeneration, associated with meningeal inflammation, could be important in determining disability progression in multiple sclerosis (MS). However, we need to know more about how cortical demyelination, neurodegeneration, and meningeal inflammation contribute to pathology at early stages of MS to better predict longterm outcome.MethodsTissue blocks from short disease duration MS (n = 12, median disease duration = 2 years), progressive MS (n = 21, disease duration = 25 years), nondiseased controls (n = 11), and other neurological inflammatory disease controls (n = 6) were quantitatively analyzed by immunohistochemistry, immunofluorescence, and in situ hybridization.ResultsCortical GM demyelination was extensive in some cases of acute MS (range = 1–48% of total cortical GM), and subpial lesions were the most common type (62%). The numbers of activated (CD68+) microglia/macrophages were increased in cases with subpial lesions, and the density of neurons was significantly reduced in acute MS normal appearing and lesion GM, compared to controls (p < 0.005). Significant meningeal inflammation and lymphoidlike structures were seen in 4 of 12 acute MS cases. The extent of meningeal inflammation correlated with microglial/macrophage activation (p < 0.05), but not the area of cortical demyelination, reflecting the finding that lymphoidlike structures were seen adjacent to GM lesions as well as areas of partially demyelinated/remyelinated, cortical GM.InterpretationOur findings demonstrate that cortical demyelination, neuronal loss, and meningeal inflammation are notable pathological hallmarks of acute MS and support the need to identify early biomarkers of this pathology to better predict outcome. Ann Neurol 2018;84:829–842
AU  - Bevan,RJ
AU  - Evans,R
AU  - Griffiths,L
AU  - Watkins,LM
AU  - Rees,MI
AU  - Magliozzi,R
AU  - Allen,I
AU  - McDonnell,G
AU  - Kee,R
AU  - Naughton,M
AU  - Fitzgerald,DC
AU  - Reynolds,R
AU  - Neal,JW
AU  - Howell,OW
DO  - 10.1002/ana.25365
EP  - 842
PY  - 2018///
SN  - 0364-5134
SP  - 829
TI  - Meningeal inflammation and cortical demyelination in acute multiple sclerosis
T2  - Annals of Neurology
UR  - http://dx.doi.org/10.1002/ana.25365
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000454104200004&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - http://hdl.handle.net/10044/1/71889
VL  - 84
ER  -
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