Brain Advance Access originally published online on August 18, 2006
Brain 2006 129(12):3165-3172; doi:10.1093/brain/awl217
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Remyelination is extensive in a subset of multiple sclerosis patients
1 Center for Brain Research, Medical University of Vienna Vienna, Austria 2 Department of Neurology, Municipal Hospital Lainz Vienna, Austria 3 Department of Neuropathology, University of Goettingen Goettingen, Germany 4 Laboratory of Neuropathology Rigshospitalet 5 Department of Neurology, University of Copenhagen Denmark 6 Department of Neurology, Mayo Clinic Rochester, Minnesota, USA
Correspondence to: Prof. Dr Hans Lassmann, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Wien, Austria E-mail: hans.lassmann{at}meduniwien.ac.at
Although spontaneous remyelination does occur in multiple sclerosis lesions, its extent within the global population with this disease is presently unknown. We have systematically analysed the incidence and distribution of completely remyelinated lesions (so-called shadow plaques) or partially remyelinated lesions (shadow plaque areas) in 51 autopsies of patients with different clinical courses and disease durations. The extent of remyelination was variable between cases. In 20% of the patients, the extent of remyelination was extensive with 6096% of the global lesion area remyelinated. Extensive remyelination was found not only in patients with relapsing multiple sclerosis, but also in a subset of patients with progressive disease. Older age at death and longer disease duration were associated with significantly more remyelinated lesions or lesion areas. No correlation was found between the extent of remyelination and either gender or age at disease onset. These results suggest that the variable and patient-dependent extent of remyelination must be considered in the design of future clinical trials aimed at promoting CNS repair.
Key Words: multiple sclerosis; remyelination; shadow plaques
Abbreviations: MBP, myelin basic protein; PLP, proteolipid protein
Received March 31, 2006. Revised July 17, 2006. Accepted July 18, 2006.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
R. Zivadinov, A. T. Reder, M. Filippi, A. Minagar, O. Stuve, H. Lassmann, M. K. Racke, M. G. Dwyer, E. M. Frohman, and O. Khan Mechanisms of action of disease-modifying agents and brain volume changes in multiple sclerosis Neurology, July 8, 2008; 71(2): 136 - 144. [Abstract] [Full Text] [PDF] |
||||
![]() |
C Trebst, F Konig, R. Ransohoff, W Bruck, and M Stangel CCR5 expression on macrophages/microglia is associated with early remyelination in multiple sclerosis lesions Multiple Sclerosis, July 1, 2008; 14(6): 728 - 733. [Abstract] [PDF] |
||||
![]() |
M. Dubois-Dalcq, A. Williams, C. Stadelmann, B. Stankoff, B. Zalc, and C. Lubetzki From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases Brain, July 1, 2008; 131(7): 1686 - 1700. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Kuhlmann, V. Miron, Q. Cuo, C. Wegner, J. Antel, and W. Bruck Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis Brain, July 1, 2008; 131(7): 1749 - 1758. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Neumann, M. R. Kotter, and R. J. M. Franklin Debris clearance by microglia: an essential link between degeneration and regeneration Brain, June 20, 2008; (2008) awn109v1. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. B. Huttner, P. Janich, M. Kohrmann, J. Jaszai, F. Siebzehnrubl, I. Blumcke, M. Suttorp, M. Gahr, D. Kuhnt, C. Nimsky, et al. The Stem Cell Marker Prominin-1/CD133 on Membrane Particles in Human Cerebrospinal Fluid Offers Novel Approaches for Studying Central Nervous System Disease Stem Cells, March 1, 2008; 26(3): 698 - 705. [Abstract] [Full Text] [PDF] |
||||
![]() |
D.S. Meier, H.L. Weiner, and C.R.G. Guttmann MR Imaging Intensity Modeling of Damage and Repair In Multiple Sclerosis: Relationship of Short-Term Lesion Recovery to Progression and Disability AJNR Am. J. Neuroradiol., November 1, 2007; 28(10): 1956 - 1963. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Marik, P. A. Felts, J. Bauer, H. Lassmann, and K. J. Smith Lesion genesis in a subset of patients with multiple sclerosis: a role for innate immunity? Brain, November 1, 2007; 130(11): 2800 - 2815. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Williams, G. Piaton, M.-S. Aigrot, A. Belhadi, M. Theaudin, F. Petermann, J.-L. Thomas, B. Zalc, and C. Lubetzki Semaphorin 3A and 3F: key players in myelin repair in multiple sclerosis? Brain, October 1, 2007; 130(10): 2554 - 2565. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Herrero-Herranz, L. A. Pardo, G. Bunt, R. Gold, W. Stuhmer, and R. A. Linker Re-Expression of a Developmentally Restricted Potassium Channel in Autoimmune Demyelination: Kv1.4 Is Implicated in Oligodendroglial Proliferation Am. J. Pathol., August 1, 2007; 171(2): 589 - 598. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Nait-Oumesmar, N. Picard-Riera, C. Kerninon, L. Decker, D. Seilhean, G. U. Hoglinger, E. C. Hirsch, R. Reynolds, and A. Baron-Van Evercooren Activation of the subventricular zone in multiple sclerosis: Evidence for early glial progenitors PNAS, March 13, 2007; 104(11): 4694 - 4699. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. J. Smith Axonal protection in multiple sclerosis--a particular need during remyelination? Brain, December 1, 2006; 129(12): 3147 - 3149. [Full Text] [PDF] |
||||






