Remyelination is extensive in a subset of multiple sclerosis patients.

By Peter T. Patrikios, C. Stadelmann, A. Kutzelnigg, H. Rauschka, M. Schmidbauer, H. Laursen, P. Sørensen, Wolfgang Brück, C. Lucchinetti, Hans Lassmann. Brain : a journal of neurology, 2006

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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 60-96% 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.

Subfields: Molecular Biology, Pathology and Forensic Medicine, Rheumatology

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Citations in the corpus

Microglial physiology: unique stimuli, specialized responses. (2009, background): “Can microglia promote repair of MS lesions? Remyelination is clearly a prevalent and poorly understood attribute of MS lesions (122).”
Debris clearance by microglia: an essential link between degeneration and regeneration (2008, background): “…the regenerative event in which new myelin sheaths are restored to demyelinated axons and that can occur with impressive efficiency in experimental models and clinical disease (Ludwin, 1978, 1980; Woodruff and Franklin, 1999; Sim et al., 2002; Patrikios et al., 2006; Patani et al., 2007).”
CNS-Resident Glial Progenitor/Stem Cells Produce Schwann Cells as well as Oligodendrocytes during Repair of CNS Demyelination (2010, neutral): “…is usually mediated by oligodendrocytes and can occur efficiently and extensively after experimentally induced demyelination in animal models or during demyelinating diseases such as multiple sclerosis (MS), the most common neurological disease of young adults (Patrikios et al., 2006).”
An updated histological classification system for multiple sclerosis lesions (2016, background): “Only approximately 20% of the lesions display extensive remyelination (=so-called shadow plaques) [24, 43, 44].”
Remyelination in the CNS: from biology to therapy (2008, background): “However, even in MS, a disease that is normally associated with failed or inadequate remyelination, there is evidence that in some patients complete remyelination occurs in a significant proportion of lesion”
Pathogenic Mechanisms Associated With Different Clinical Courses of Multiple Sclerosis (2019, background): “Thus, these lesions may become inactive and a subset of them may even be repaired by remyelination (53).”
Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis. (2008, background): “Analyses of chronic multiple sclerosis lesions indicate that although remyelination may be extensive in some of them, it is absent or limited to the plaque border in the majority (Prineas and Connell, 1979; Barkhof et al., 2003; Patrikios et al., 2006; Patani et al., 2007).”
The Immunopathology of Multiple Sclerosis: An Overview (2007, background): “In addition, we found that in approximately 20% of MS patients, remyelination is so extensive that almost all plaques within the CNS are shadow plaques (70).”
Dysregulation of the Wnt pathway inhibits timely myelination and remyelination in the mammalian CNS. (2009, background): “However, although it can be extensive in MS (Patrikios et al. 2006; Patani et al. 2007), it is an inconsistent event, and the accumulated load of lesions that fail to remyelinate in a timely manner contributes to irreversible axon loss and progressive neurological deterioration (Frohman et al.…”
Clinical and Pathological Insights into the Dynamic Nature of the White Matter Multiple Sclerosis Plaque (2015, background): “Thus, the results could also mean that those shadow plaques are lesions that have been formed in early disease stages and show persistent remyelination through the subsequent course of the disease.(3,13,17,36) Observations from different studies have led to the hypothesis that the accumulation of di”