The basis for treatment in multiple sclerosis

被引:9
作者
Compston, A [1 ]
机构
[1] Univ Cambridge, Sch Clin, Dept Clin Neurosci, Cambridge CB2 2QQ, England
来源
ACTA NEUROLOGICA SCANDINAVICA | 2006年 / 113卷
关键词
multiple sclerosis; inflammation; axonal injury; remyelination; clinical course; treatment;
D O I
10.1111/j.1600-0404.2006.00614.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Contemporary licensed treatments for multiple sclerosis fail to provide a solution for the disease because their effects are limited to a modest reduction in the frequency of new episodes. They do not reduce disability or materially influence the progressive phase of the disease. A contemporary strategy for management requires a more detailed analysis of the separate contributions to the clinical features and overall course made by inflammation, axonal injury, compensatory mechanisms, and remyelination. From this formulation emerges the need either for early and fully effective suppression of the inflammatory response, limiting the damage to all components of the axon-glial unit; or the development of strategies for axonal and myelin repair that solve the issues of controlled differentiation, delivery and timing of these cell and growth factor-based interventions.
引用
收藏
页码:41 / 47
页数:7
相关论文
共 40 条
[1]   Relapsing and remitting multiple sclerosis: Pathology of the newly forming lesion [J].
Barnett, MH ;
Prineas, JW .
ANNALS OF NEUROLOGY, 2004, 55 (04) :458-468
[2]   Identification of a human olfactory ensheathing cell that can effect transplant-mediated remyelination of demyelinated CNS axons [J].
Barnett, SC ;
Alexander, CL ;
Iwashita, Y ;
Gilson, JM ;
Crowther, J ;
Clark, L ;
Dunn, LT ;
Papanastassiou, V ;
Kennedy, PGE ;
Franklin, RJM .
BRAIN, 2000, 123 :1581-1588
[3]   Compact myelin dictates the differential targeting of two sodium channel isoforms in the same axon [J].
Boiko, T ;
Rasband, MN ;
Levinson, SR ;
Caldwell, JH ;
Mandel, G ;
Trimmer, JS ;
Matthews, G .
NEURON, 2001, 30 (01) :91-104
[4]   LIF receptor signaling limits immune-mediated demyelination by enhancing oligodendrocyte survival [J].
Butzkueven, H ;
Zhang, JG ;
Hanninen, MS ;
Hochrein, H ;
Chionh, F ;
Shipham, KA ;
Emery, B ;
Turnley, AM ;
Petratos, S ;
Ernst, M ;
Bartlett, PF ;
Kilpatrick, TJ .
NATURE MEDICINE, 2002, 8 (06) :613-619
[5]   The neuregulin, glial growth factor 2, diminishes autoimmune demyelination and enhances remyelination in a chronic relapsing model for multiple sclerosis [J].
Cannella, B ;
Hoban, CJ ;
Gao, YL ;
Garcia-Arenas, R ;
Lawson, D ;
Marchionni, M ;
Gwynne, D ;
Raine, CS .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (17) :10100-10105
[6]  
Coles AJ, 1999, ANN NEUROL, V46, P296, DOI 10.1002/1531-8249(199909)46:3<296::AID-ANA4>3.0.CO
[7]  
2-#
[8]   The window of therapeutic opportunity in multiple sclerosis [J].
Coles, AJ ;
Cox, A ;
Le Page, E ;
Jones, J ;
Trip, SA ;
Deans, J ;
Seaman, S ;
Miller, DH ;
Hale, G ;
Waldmann, H ;
Compston, DA .
JOURNAL OF NEUROLOGY, 2006, 253 (01) :98-108
[9]   Relapses and progression of disability in multiple sclerosis. [J].
Confavreux, C ;
Vukusic, S ;
Moreau, T ;
Adeleine, P .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 343 (20) :1430-1438
[10]   Reply to: Age at disability milestones in multiple sclerosis and history of multiple sclerosis: a unifying concept [J].
Confavreux, Christian ;
Vukusic, Sandra .
BRAIN, 2006, 129