Experimental models of multiple sclerosis

被引:63
作者
Pachner, Andrew R. [1 ]
机构
[1] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Neurol & Neurosci, Newark, NJ 07103 USA
关键词
animal models; autoimmunity; demyelination; multiple sclerosis; virus; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; THEILERS-VIRUS-INFECTION; MYELIN OLIGODENDROCYTE GLYCOPROTEIN; B-CELL DEPLETION; DEMYELINATING DISEASE; NEUROMYELITIS-OPTICA; VIRAL REPLICATION; IMMUNE-RESPONSES;
D O I
10.1097/WCO.0b013e328346c226
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Purpose of review Multiple sclerosis (MS) is a disease of the central nervous system of unknown cause. There are many medications available for the disease, but none are clearly effective in ameliorating its long-term disabling effects. MS is felt to be most likely either due to an aberrant immune response or a pathogen, or possibly a combination of the two, and the animal models available reflect these two possible pathogeneses. The hallmarks of the disease are demyelination, inflammation, axonal injury, and progressive disability. This review explores the experimental models of multiple sclerosis. Recent findings There are a variety of forms of experimental allergic encephalomyelitis, the most commonly studied animal model of MS. Two viruses, Theiler's murine encephalomyelitis virus and murine hepatitis virus, are used to induce infectious models of the disease. Summary The animal models have their advantages and disadvantages, but no model fully reproduces the spectrum of the human disease.
引用
收藏
页码:291 / 299
页数:9
相关论文
共 62 条
[31]   Axonal loss results in spinal-cord atrophy, electrophysiological abnormalities and neurological deficits following demyelination in a chronic inflammatory model of multiple sclerosis [J].
McGavern, DB ;
Murray, PD ;
Rivera-Quiñones, C ;
Schmelzer, JD ;
Low, PA ;
Rodriguez, M .
BRAIN, 2000, 123 :519-531
[32]  
Meinl E., 2010, Journal of the neurological sciences
[33]   Compartmentalization of inflammation in the CNS: A major mechanism driving progressive multiple sclerosis [J].
Meinl, Edgar ;
Krumbholz, Markus ;
Derfuss, Tobias ;
Junker, Andreas ;
Hohlfeld, Reinhard .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 2008, 274 (1-2) :42-44
[34]   Animal models of multiple sclerosis-Potentials and limitations [J].
Mix, Eilhard ;
Meyer-Rienecker, Hans ;
Hartung, Hans-Peter ;
Zettl, Uwe K. .
PROGRESS IN NEUROBIOLOGY, 2010, 92 (03) :386-404
[35]   1,026 experimental treatments in acute stroke [J].
O'Collins, VE ;
Macleod, MR ;
Donnan, GA ;
Horky, LL ;
van der Worp, BH ;
Howells, DW .
ANNALS OF NEUROLOGY, 2006, 59 (03) :467-477
[36]   Microglia initiate central nervous system innate and adaptive immune responses through multiple TLRs [J].
Olson, JK ;
Miller, SD .
JOURNAL OF IMMUNOLOGY, 2004, 173 (06) :3916-3924
[37]   Antibody-secreting cells in the central nervous system in an animal model of MS: Phenotype, association with disability, and in vitro production of antibody [J].
Pachner, Andrew R. ;
Brady, Jennifer ;
Narayan, Kavitha .
JOURNAL OF NEUROIMMUNOLOGY, 2007, 190 (1-2) :112-120
[38]   Intrathecal antibody production in an animal model of multiple sclerosis [J].
Pachner, Andrew R. ;
Li, Libin ;
Narayan, Kavitha .
JOURNAL OF NEUROIMMUNOLOGY, 2007, 185 (1-2) :57-63
[39]   Plasma cells in the central nervous system in the Theiler's virus model of multiple sclerosis [J].
Pachner, Andrew R. ;
Li, Libin ;
Lagunoff, David .
JOURNAL OF NEUROIMMUNOLOGY, 2011, 232 (1-2) :35-40
[40]   Changes in B- and T-Lymphocyte and Chemokine Levels With Rituximab Treatment in Multiple Sclerosis [J].
Piccio, Laura ;
Naismith, Robert T. ;
Trinkaus, Kathryn ;
Klein, Robyn S. ;
Parks, Becky J. ;
Lyons, Jeri A. ;
Cross, Anne H. .
ARCHIVES OF NEUROLOGY, 2010, 67 (06) :707-714