An experimental model of secondary progressive multiple sclerosis that shows regional variation in gliosis, remyelination, axonal and neuronal loss

被引：52

作者：

Hampton, David W. ^{[1
]}

Anderson, Jane ^{[1
]}

Pryce, Gareth ^{[2
]}

Irvine, Karen-Amanda ^{[4
]}

Giovannoni, Gavin ^{[2
]}

Fawcett, James W. ^{[1
]}

Compston, Alastair ^{[1
]}

Franklin, Robin J. M. ^{[1
,3
]}

Baker, David ^{[2
]}

Chandran, Siddharthan ^{[1
]}

机构：

[1] Univ Cambridge, Cambridge Ctr Brain Repair, Cambridge CB2 2PY, England

[2] Queen Mary Univ London, Inst Cell & Mol Sci, Ctr Neurosci, London E1 2AT, England

[3] Univ Cambridge, Dept Vet Med, Cambridge CB3 0ES, England

[4] Univ Calif San Francisco, Dept Neurol Surg, Brain & Spinal Injury Ctr, San Francisco, CA 94110 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2008年 / 201卷

关键词：

Experimental autoimmune encephalomyelitis; Multiple sclerosis; Remyelination; Gliosis; Axon;

D O I：

10.1016/j.jneuroim.2008.05.034

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Multiple sclerosis (MS) represents a considerable challenge to experimentally model due to its twin pathologies of inflammatory demyelination and neurodegeneration along with its multifocal and multiphasic nature. Experimental autoimmune encephalomyelitis ( I EAE) in Biozzi ABH mice has previously been shown to reproduce Many clinical features also found in secondary progressive MS. In this Study we sought to characterise the pathology of chronic EAE in ABH mice. In addition to Marked gliosis, we report Substantial demyelination, remyelination and axonal and neuronal loss, Together with the clinical pattern, Our findings identify chronic EAE as an excellent model of secondary progressive Multiple sclerosis. (c) 2008 Elsevier B.V All rights reserved.

引用

页码：200 / 211

页数：12

共 57 条

[11] Thalamic neurodegeneration in multiple sclerosis [J].

Cifelli, A ;

Arridge, M ;

Jezzard, P ;

Esiri, MM ;

Palace, J ;

Matthews, PM .

ANNALS OF NEUROLOGY, 2002, 52 (05) :650-653

[12]

Coles AJ, 1999, ANN NEUROL, V46, P296, DOI 10.1002/1531-8249(199909)46:3<296::AID-ANA4>3.0.CO

[13]

2-#

[14] Multiple sclerosis [J].

Compston, A ;

Coles, A .

LANCET, 2002, 359 (9313) :1221-1231

[15] Optimization of an animal model of experimental autoimmune encephalomyelitis achieved with a multiple MOG35-55 peptide in C57BL6/J strain of mice [J].

Costa, O ;

Divoux, D ;

Ischenko, A ;

Tron, F ;

Fontaine, M .

JOURNAL OF AUTOIMMUNITY, 2003, 20 (01) :51-61

[16] Axonal loss in multiple sclerosis: a pathological survey of the corticospinal and sensory tracts [J].

DeLuca, GC ;

Ebers, GC ;

Esiri, MM .

BRAIN, 2004, 127 :1009-1018

[17] Inflammation stimulates remyelination in areas of chronic demyelination [J].

Foote, AK ;

Blakemore, WF .

BRAIN, 2005, 128 :528-539

[18]

Franklin R J, 2001, Prog Brain Res, V132, P185

[19] Why does remyelination fail in multiple sclerosis? [J].

Franklin, RJM .

NATURE REVIEWS NEUROSCIENCE, 2002, 3 (09) :705-714

[20] Medical progress: Multiple sclerosis - The plaque and its pathogenesis [J].

Frohman, EM ;

Racke, MK ;

Raine, CS .

NEW ENGLAND JOURNAL OF MEDICINE, 2006, 354 (09) :942-955

← 1 2 3 4 5 6 →