Original Article
Premyelinating Oligodendrocytes in Chronic Lesions of Multiple Sclerosis
N Engl J Med 2002; 346:165-173January 17, 2002
- Abstract
Background
Multiple sclerosis is an inflammatory disease of the central nervous system that destroys myelin, oligodendrocytes, and axons. Since most of the lesions of multiple sclerosis are not remyelinated, enhancement of remyelination is a possible therapeutic strategy that could perhaps be achieved with the transplantation of oligodendrocyte-producing cells into the lesions. We investigated the frequency distribution and configuration of oligodendrocytes in chronic lesions of multiple sclerosis to determine whether these factors limit remyelination.
Methods
Forty-eight chronic lesions obtained at autopsy from 10 patients with multiple sclerosis were examined immunocytochemically for oligodendrocytes and oligodendrocyte progenitor cells. Using confocal microscopy, we examined the three-dimensional relations between axons and the processes of premyelinating oligodendrocytes.
Results
Thirty-four of the 48 chronic lesions of multiple sclerosis contained oligodendrocytes with multiple extended processes that associated with demyelinated axons but failed to myelinate them. These axons were dystrophic and contained multiple swellings. In some regions, the densities of premyelinating oligodendrocytes (25 per square millimeter of tissue) were similar to those in the developing rodent brain (23 per square millimeter). In the patients with disease of long duration (more than 20 years), there were fewer lesions with premyelinating oligodendrocytes (P<0.001).
Conclusions
Premyelinating oligodendrocytes are present in chronic lesions of multiple sclerosis, so remyelination is not limited by an absence of oligodendrocyte progenitors or their failure to generate oligodendrocytes. Our findings suggest that in the chronic lesions of multiple sclerosis, the axons are not receptive for remyelination. Understanding the cellular interactions between premyelinating oligodendrocytes, axons, and the microenvironment of lesions of multiple sclerosis may lead to effective strategies for enhancing remyelination.
Media in This Article
Figure 3
Oligodendrocyte Progenitor Cells in Chronic Lesions of Multiple Sclerosis.Figure 2
Scatter Plot of the Density of Premyelinating Oligodendrocytes in the Total Areas of Chronic Lesions, in Lesion Areas Enriched in Premyelinating Oligodendrocytes, and in Rat Cerebral Cortex (Postnatal Day 14).Article Activity
- Article
Multiple sclerosis is an inflammatory disease of the central nervous system that destroys myelin, the insulation that surrounds axons. Oligodendrocytes (the cells that produce myelin) and nerve fibers are also destroyed.1-4 Most patients with multiple sclerosis have an initial relapsing–remitting course for 5 to 15 years that then takes a secondary progressive course of irreversible neurologic disability.5 Relapses result from inflammation and demyelination, whereas restoration of nerve conduction and remission is accompanied by resolution of inflammation, redistribution of sodium channels on demyelinated axons, and remyelination.6,7
Demyelination is not always permanent in multiple sclerosis. Remyelination during early stages of the disease process has been documented by histologic analysis of tissue specimens from both biopsy and postmortem examination.8-11 Most chronic lesions of multiple sclerosis, however, are not remyelinated. Remyelination requires generation of new oligodendrocytes.12 Oligodendrocyte progenitor cells, identified by the expression of the platelet-derived growth factor receptor α and the sulfated proteoglycan NG2, have been characterized in developing brain,13,14 normal adult human brain,15-17 and chronic lesions of multiple sclerosis.16,18,19 Isolated progenitor cells can give rise to oligodendrocytes in vitro.20-23 During development of the rodent brain, oligodendrocyte progenitor cells differentiate into premyelinating oligodendrocytes that radially extend multiple processes positive for myelin proteins that do not immediately myelinate axons.24 These premyelinating oligodendrocytes have a limited life span (approximately three days) and either myelinate axons or die by programmed cell death.24,25 Premyelinating oligodendrocytes are not detected in white matter in the brains of normal adult rodents or humans.
Transplantation of oligodendrocyte-producing cells into lesions of multiple sclerosis is being considered as a therapeutic strategy to enhance remyelination.26 It remains to be determined, however, whether oligodendrocyte progenitors or production or differentiation of oligodendrocytes limits remyelination in chronic lesions of multiple sclerosis. Despite detection of cells with phenotypic characteristics of oligodendrocyte progenitor cells in chronic lesions of multiple sclerosis,16,18,19 the potential for these cells to produce oligodendrocytes has not been demonstrated. This report describes oligodendrocytes in chronic lesions of multiple sclerosis that extend multiple processes that associate with but fail to myelinate axons.
Methods
Tissue
The brains from 10 deceased patients with multiple sclerosis were investigated. Six brains were obtained from patients who had been followed at the Cleveland Clinic Foundation. These brains were sliced (1 cm thick) and fixed in 4 percent paraformaldehyde. Lesions were removed, cryoprotected, and sectioned (30 μm thick) on a freezing–sliding microtome. Fresh-frozen brain slices from four other deceased patients with multiple sclerosis were obtained from the Multiple Sclerosis Human Neurospecimen Bank in Los Angeles and were simultaneously thawed and fixed in 4 percent paraformaldehyde and processed as described above. Clinical data for the patients are summarized in Table 1Table 1
Characteristics of Patients and Lesions Studied..Patient 1 died from respiratory failure accompanying severe brain-stem inflammation in the setting of relapsing multiple sclerosis. All the other patients died of medical complications from severe, debilitating multiple sclerosis, as listed in Table 1. Two patients received disease-modifying therapy in the year before death. Patient 1 was treated with cyclophosphamide and methylprednisolone one month before death; Patient 7 was receiving interferon beta treatment at the time of death. On the basis of the distribution of myelin protein and the staining for major-histocompatibility-complex (MHC) class II molecules, 52 lesions were identified and classified as active (4), chronic active (5), and chronic inactive (43), as described previously.4
Immunocytochemical Analysis
Free-floating sections (30 μm thick) were microwaved in 10 mM citric acid buffer (pH 6.0) twice for 5 minutes, incubated in 1 percent hydrogen peroxide and 10 percent Triton X-100 in phosphate-buffered saline for 30 minutes, and immunostained by the avidin–biotin complex procedure with diaminobenzidine, as described previously.24 Sections were incubated in proteolipid-protein antibodies for five days at 4°C. Sections stained for NG2 were not microwaved; they were pretreated with 0.3 percent Triton X-100 and immunostained with the use of the tyramide signal-amplification method (PerkinElmer Life Sciences, Boston), as previously described.16 Sections for double labeling were pretreated as above and incubated with two primary antibodies for five days and with fluorescein-conjugated and biotinylated secondary antibodies (Jackson ImmunoResearch Laboratories, West Grove, Pa.) for one hour.
Antibodies
Sections were immunostained with the following antibodies: rat anti–proteolipid protein (Agmed, Bedford, Mass.), mouse anti–myelin oligodendrocyte glycoprotein (a gift from Dr. Minnetta Gardinier, University of Iowa, Iowa City), mouse anti–human NG2 (clone 9.2.27, Pharmingen, San Diego, Calif.), mouse anti–human MHC class II (Dako, Glostrup, Denmark), mouse anti–nonphosphorylated neurofilament (SMI32, Sternberger Monoclonals, Baltimore), mouse anti–phosphorylated neurofilament (SMI31, Sternberger Monoclonals), and rabbit antineurofilament (Serotec, Raleigh, N.C.).
Confocal Microscopy
Sections were examined with a laser scanning confocal microscope (Leica Microsystems, Exton, Pa.). Antibody combinations included proteolipid protein plus neurofilament and myelin oligodendrocyte glycoprotein plus neurofilament. Laser intensity was adjusted to eliminate “bleed-through.” The images presented are stacks of 18 to 36 optical sections that were scanned synchronously.
Quantification of Premyelinating Oligodendrocytes
Premyelinating oligodendrocytes in lesions of multiple sclerosis were identified as cells positive for proteolipid protein with multiple processes that did not contact myelin internodes. To determine the size of the demyelinated area, sections stained with proteolipid protein antibodies were scanned (ScanMaker 4, Microtek Lab, Redondo Beach, Calif.); the borders of the lesions were outlined on a digital image, and the demyelinated area was measured with software from the National Institutes of Health (NIH Image). The density of premyelinating oligodendrocytes was determined in the total demyelinated area in 34 lesions, in 30 lesions enriched in premyelinating oligodendrocytes, and in developing rat brain (postnatal day 14). Areas of lesions of multiple sclerosis containing more than six premyelinating oligodendrocytes per 0.38 mm2 were calculated separately and classified as enriched in premyelinating oligodendrocytes; this density was chosen because it is similar to that found in areas of the developing rodent brain. The density of premyelinating oligodendrocytes in developing rat brain was determined by counting 15 regions of unmyelinated cerebral cortex. Densities of premyelinating oligodendrocytes were compared by Student's t-test. The relation between the percentage of lesions with premyelinating oligodendrocytes and the duration of disease, the age of the patient at the time of death, the type of disease, and the score on the Expanded Disability Status Scale (EDSS; possible range, 0 to 10, with a higher score indicating a greater degree of disability)27 was determined by the Pearson correlation coefficient.
Results
Premyelinating Oligodendrocytes in Chronic Lesions of Multiple Sclerosis
The clinical history and number of lesions studied from each patient are shown in Table 1. Forty-eight chronic lesions of multiple sclerosis from 10 deceased patients with multiple sclerosis were examined for oligodendrocytes. Chronic lesions of multiple sclerosis were identified by the presence of demyelination and a low density of cells positive for MHC class II molecules (insets in Figure 1AFigure 1
Premyelinating Oligodendrocytes in Chronic Lesions of Multiple Sclerosis.). Premyelinating oligodendrocytes were detected in 34 lesions (71 percent). These premyelinating oligodendrocytes were not evenly distributed within the lesions and tended to occur in groups (Figure 1A). The general morphologic appearance of the cells varied, depending on location. The perikarya of the premyelinating oligodendrocytes were often detected in the axon-free subventricular zone (Figure 1B and Figure 1C). These cells asymmetrically extended multiple processes positive for proteolipid protein into the area of demyelinated axons. Most premyelinating oligodendrocytes were clustered throughout the lesions (inset in Figure 1D) and radially extended multiple processes positive for proteolipid protein that were oriented parallel to demyelinated axons (Figure 1D).In the 34 chronic lesions with premyelinating oligodendrocytes, the average density of premyelinating oligodendrocytes was 2 per square millimeter (Figure 2Figure 2
Scatter Plot of the Density of Premyelinating Oligodendrocytes in the Total Areas of Chronic Lesions, in Lesion Areas Enriched in Premyelinating Oligodendrocytes, and in Rat Cerebral Cortex (Postnatal Day 14).). However, in 30 lesion areas enriched in premyelinating oligodendrocytes, the density of oligodendrocytes (25 per square millimeter) was similar to that found in developing rat brain (23 per square millimeter) (Figure 2). Thirteen of the 30 areas were located close to the subventricular zone. In the 34 lesions analyzed, premyelinating oligodendrocytes were enriched in approximately 7 percent of the total area of the lesions.Fourteen of the 48 chronic lesions studied did not contain detectable premyelinating oligodendrocytes (Table 1). Eleven lesions without premyelinating oligodendrocytes came from the three patients with the longest duration of disease (23, 35, and 44 years), whereas only 1 of 14 lesions from Patient 6 was negative for premyelinating oligodendrocytes. The percentage of lesions with premyelinating oligodendrocytes varied inversely with the duration of disease (Pearson correlation coefficient, –0.90; 95 percent confidence interval, –0.62 to –0.98; P<0.001). The age of the patient at the time of death, the type of disease, and the EDSS score did not correlate with the percentage of lesions with premyelinating oligodendrocytes (P>0.05).
Oligodendrocyte Progenitor Cells in Chronic Lesions of Multiple Sclerosis
Cells expressing the sulfated proteoglycan NG2 may be oligodendrocyte progenitor cells in lesions of multiple sclerosis.16 The distribution of NG2-positive cells was investigated in sections cut adjacent to sections stained with proteolipid protein antibodies. Subventricular areas of the lesions with premyelinating oligodendrocytes contained stellate NG2 cells (Figure 3AFigure 3
Oligodendrocyte Progenitor Cells in Chronic Lesions of Multiple Sclerosis.) that had an appearance similar to that of NG2 cells in brains from deceased patients without neurologic disease. As in these brains, many of the NG2-positive cells projected processes to blood vessels that were also NG2-positive. Other regions of the lesions of multiple sclerosis enriched in premyelinating oligodendrocytes contained elongated (Figure 3A) or stellate (Figure 3B) NG2 cells.Stellate NG2 cells were detected in lesions without premyelinating oligodendrocytes. The density of these cells, however, was less than that in nonlesion areas of the same sections. In addition, these NG2 cells had fewer, shorter, and thicker processes than those in nonlesion areas (Figure 3C). Elongated NG2 cells were not detected in lesions without premyelinating oligodendrocytes.
Processes of Premyelinating Oligodendrocytes Associated with Axons
The orientation of processes of premyelinating oligodendrocytes (Figure 1) suggests that they physically associate with demyelinated axons. This possibility was investigated by determining the three-dimensional relation between processes of premyelinating oligodendrocytes and axons in confocal images of sections immunostained with proteolipid protein and neurofilament antibodies. Figure 4AFigure 4
Processes of Premyelinating Oligodendrocytes Associated with Axons. shows a premyelinating oligodendrocyte located in the axon-free subventricular zone. This cell extended processes positive for proteolipid protein into the zone of demyelinated axons. When these processes reached the demyelinated axons, many assumed a parallel orientation with individual axons (Figure 4A). Three-dimensional analysis of rotated images indicated that many processes longitudinally spiraled around axons (Figure 4B). Radial ensheathment of axons, however, was rare.During normal development of the rodent brain, myelin oligodendrocyte glycoprotein is considered a marker of mature or myelinating oligodendrocytes28 and has not been detected in premyelinating oligodendrocytes (unpublished data). Many premyelinating oligodendrocytes in chronic lesions of multiple sclerosis, however, were stained by myelin oligodendrocyte glycoprotein antibodies (Figure 4C). Perikarya of premyelinating oligodendrocytes located within lesions radially extended processes that also associated with individual axons (Figure 4D). Some processes extended considerable distances before associating with axons, and many axons close to oligodendrocyte-cell bodies were not ensheathed by oligodendrocyte processes. Dying premyelinating oligodendrocytes, which were characterized by fragmented processes, condensed perinuclear cytoplasm, and nuclei stained for proteolipid protein (inset in Figure 4D), were also detected in chronic lesions of multiple sclerosis.
Oligodendrocytes in Remyelinating Lesions
Previous studies identified abundant oligodendrocytes in some subacute lesions of multiple sclerosis.11,29 These oligodendrocytes extended a few short processes, but they did not myelinate axons. Four acute lesions with abundant macrophages that were positive for MHC class II molecules contained regions with abundant, small, round oligodendrocytes with few or no processes (data not shown). Premyelinating oligodendrocytes with multiple radially oriented processes were not detected in these acute lesions. Remyelination was evident, however, at the edge of many chronic lesions. The relation between remyelinating oligodendrocytes and axons was investigated by confocal microscopy in these partially remyelinated lesions or “shadow plaques.”
Remyelinating oligodendrocytes had relatively large perikarya positive for proteolipid protein and extended processes to short myelin internodes (Figure 5AFigure 5
Remyelinating Oligodendrocytes in Chronic Lesions of Multiple Sclerosis.). The number of processes was often matched to the number of internodes, particularly in remyelinating oligodendrocytes that formed longer internodes (Figure 5B). In areas of shadow plaque with more remyelination and longer internodes, oligodendrocyte perikarya were smaller and less intensely stained by proteolipid-protein antibodies (Figure 5C) than in premyelinating oligodendrocytes (Figure 1B, Figure 1C, Figure 1D, and Figure 4D) or in early remyelinating oligodendrocytes (Figure 5A and Figure 5B). Oligodendrocyte processes extending to myelin internodes were not always detected within shadow plaques. Premyelinating oligodendrocytes were not detected in shadow plaques of the chronic lesions of multiple sclerosis that we analyzed.The morphologic appearance of axons in chronic lesions containing premyelinating oligodendrocytes and remyelinating oligodendrocytes differed. Chronic lesions with premyelinating oligodendrocytes contained axons (Figure 4A, Figure 4B, and Figure 4C) with multiple swellings, marked variations in diameter, and a more tortuous course. In contrast, remyelinated axons (Figure 5B and Figure 5C) were straight, with relatively consistent diameters. The edge of shadow plaques often contained a combination of dystrophic and healthy-appearing axons (Figure 5A). In general, the majority of remyelinated internodes surrounded the healthy-appearing axons.
Discussion
In the central nervous system of patients with multiple sclerosis, remyelination may be able to restore rapid nerve conduction and protect demyelinated axons from degeneration. To develop strategies for successful remyelination, one needs to identify why remyelination fails. We detected premyelinating oligodendrocytes in 34 of 48 chronic lesions of multiple sclerosis, which establishes that some other factors limit remyelination of such lesions. The premyelinating oligodendrocytes physically associated with axons and were abundant in patients with clinical disease of 1 to 15 years' duration. This provides an extended window of opportunity to deliver remyelinating therapeutic agents that target premyelinating oligodendrocytes, the microenvironment of chronic lesions of multiple sclerosis, or both.
The differentiation of oligodendrocytes in chronic lesions of multiple sclerosis appears to recapitulate the premyelinating stage identified during the development of the rodent brain.24 The positive correlation between the distribution of NG2 cells and premyelinating oligodendrocytes suggests that NG2 cells are a source of these premyelinating oligodendrocytes. It remains to be determined whether premyelinating oligodendrocytes are generated from a stem or progenitor cell that repopulates the lesion or from the NG2 cells in or near the lesion. In either event, the detection of premyelinating oligodendrocytes unequivocally establishes the presence of oligodendrocyte progenitor cells in chronic lesions of multiple sclerosis. All patients examined had lesions with premyelinating oligodendrocytes (Table 1). It remains to be determined, however, whether proposed variations in the pathogenesis of multiple sclerosis30 will affect the number of premyelinating oligodendrocytes in chronic lesions. Fourteen chronic lesions were negative for premyelinating oligodendrocytes. Eleven of these lesions were from patients with disease of more than 20 years' duration, suggesting that chronic lesions eventually lose the ability to maintain or produce new oligodendrocytes.
We confirmed previous reports11,31-33 describing abundant, small, round oligodendrocytes that were positive for myelin oligodendrocyte glycoprotein in acute lesions of multiple sclerosis. Although premyelinating oligodendrocytes were not detected immunocytochemically in previous studies, cells positive for proteolipid protein messenger RNA were detected by in situ hybridization in tissue sections of chronic lesions of multiple sclerosis11,31,32 and are likely to represent, at least in part, the premyelinating oligodendrocytes identified in the present report. Optimal immunocytochemical detection of premyelinating oligodendrocytes in developing brain24 or lesions of multiple sclerosis (Figure 1, Figure 4, and Figure 5) requires microwave pretreatment and five days of incubation with primary antibody. In addition, resolution of elaborate processes, the morphologic hallmark of premyelinating oligodendrocytes, is best achieved in sections of 30 μm or thicker. As in other studies, we have not detected premyelinating oligodendrocytes with more conventional staining procedures.
The remyelinating potential of premyelinating oligodendrocytes in chronic lesions of multiple sclerosis will depend on the life span of the cells. Although it is impossible to determine the life spans of cells in the human brain, the detection of apoptotic premyelinating oligodendrocytes in chronic lesions of multiple sclerosis (inset in Figure 4D) indicates that their life spans are limited. If the life span is two to three days, as reported for the developing rodent central nervous system,25,34 the total number of oligodendrocytes produced in chronic lesions that are years or decades old should be more than enough to remyelinate the lesions. Rodent premyelinating oligodendrocytes that are produced in the absence of axons of the optic nerve extend fewer and shorter processes than those in normal nerves35 or in chronic lesions of multiple sclerosis (Figure 1 and Figure 4). Axons in the chronic lesions of multiple sclerosis therefore appear capable of supporting differentiation of an oligodendrocyte to a premyelinating phenotype, to association with axons, and to expression of myelin oligodendrocyte glycoprotein, but not to myelination.
Little is known about the molecular mechanisms responsible for the initiation of myelination or whether the inhibition of myelination in lesions of multiple sclerosis is due to dysregulated growth factors, the altered molecular composition of axons, or the presence of an inhibitory signal. The correlation between dystrophic axons with swellings and lesions with premyelinating oligodendrocytes but no remyelination supports the hypothesis that axonal pathologic processes limit the remyelination of chronic lesions of multiple sclerosis. This hypothesis is also supported by data in animals36-38 and the morphologic integrity of remyelinated axons in shadow plaques described here and in previous studies.37 At present, there is no evidence of genetic defects specific for oligodendrocytes that would limit remyelination in patients with multiple sclerosis.
With regard to possible remyelination therapies, an important question is whether transplantation of the appropriate cell into lesions of multiple sclerosis would promote remyelination. Our data indicate that the environment of many chronic inactive lesions of multiple sclerosis supports the production of new premyelinating oligodendrocytes from endogenous cell populations and suggest that it would support such production from transplanted progenitor cells. However, it appears that the environment within chronic lesions will not provide the appropriate signals for remyelination. We speculate that failure of remyelination by premyelinating oligodendrocytes in chronic lesions of multiple sclerosis is due to an abnormal molecular composition of chronically demyelinated axons or an imbalance of growth factors that regulate myelination. The challenge is therefore to understand the interactions between premyelinating cells, axons, and the microenvironment of the lesions better. If lesions of multiple sclerosis can be modified to promote the myelination of axons by processes of premyelinating oligodendrocytes, cell transplantation into chronic lesions could prove beneficial.
Supported by grants (PO1 NS38667 and RO1 NS35058) from the National Institutes of Health.
We are indebted to the Cleveland Clinic Foundation Multiple Sclerosis Tissue Donation Program and the Multiple Sclerosis Human Neurospecimen Bank for providing tissue specimens; to Drs. Richard Ransohoff, Jeff Cohen, and Robert Miller for helpful comments; to Dr. Grahame Kidd for confocal-image analysis; to Renata Klinkosz for technical help; and to Victoria Pickett for editorial assistance.
Source Information
From the Department of Neurosciences, Lerner Research Institute (A.C., B.D.T.), and the Mellen Center for Multiple Sclerosis (R.R.), Cleveland Clinic Foundation, Cleveland; and the Department of Neurology, West Los Angeles Veterans Affairs Medical Center, Los Angeles (W.W.T.).
Address reprint requests to Dr. Trapp at the Department of Neurosciences, NC30, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195, or at trappb@ccf.org.
- References
References
1
Noseworthy JH ,Lucchinetti C ,Rodriguez M ,Weinshenker BG . Multiple sclerosis. N Engl J Med 2000;343:938-952
Full Text | Web of Science | Medline2
Raine CS . Multiple sclerosis: immune system molecule expression in the central nervous system. J Neuropathol Exp Neurol 1994;53:328-337
CrossRef | Web of Science | Medline3
Ferguson B ,Matyszak MK ,Esiri MM ,Perry VH . Axonal damage in acute multiple sclerosis lesions. Brain 1997;120:393-399
CrossRef | Web of Science | Medline4
Trapp BD ,Peterson J ,Ransohoff RM ,Rudick R ,Mork S ,Bo L . Axonal transection in the lesions of multiple sclerosis. N Engl J Med 1998;338:278-285
Full Text | Web of Science | Medline5
Weinshenker BG ,Bass B ,Rice GP , et al. The natural history of multiple sclerosis: a geographically based study. I. Clinical course and disability. Brain 1989;112:133-146
CrossRef | Web of Science | Medline6
Waxman SG . Demyelinating diseases -- new pathological insights, new therapeutic targets. N Engl J Med 1998;338:323-325
Full Text | Web of Science | Medline7
Trapp BD ,Ransohoff RM ,Fisher E ,Rudick RA . Neurodegeneration in multiple sclerosis: relationship to neurological disability. Neuroscientist 1999;5:48-57
CrossRef | Web of Science8
Prineas JW ,Connell F . Remyelination in multiple sclerosis. Ann Neurol 1979;5:22-31
CrossRef | Web of Science | Medline9
Prineas JW ,Kwon EE ,Cho ES ,Sharer LR . Continual breakdown and regeneration of myelin in progressive multiple sclerosis plaques. Ann N Y Acad Sci 1984;436:11-32
CrossRef | Web of Science | Medline10
Raine CS ,Wu E . Multiple sclerosis: remyelination in acute lesions. J Neuropathol Exp Neurol 1993;52:199-204
CrossRef | Web of Science | Medline11
Lucchinetti C ,Bruck W ,Parisi J ,Scheithauer B ,Rodriguez M ,Lassmann H . A quantitative analysis of oligodendrocytes in multiple sclerosis lesions: a study of 113 cases. Brain 1999;122:2279-2295
CrossRef | Web of Science | Medline12
Keirstead HS ,Blakemore WF . Identification of post-mitotic oligodendrocytes incapable of remyelination within the demyelinated adult spinal cord. J Neuropathol Exp Neurol 1997;56:1191-1201
CrossRef | Web of Science | Medline13
Nishiyama A ,Lin XH ,Giese N ,Heldin CH ,Stallcup WB . Co-localization of NG2 proteoglycan and PDGF α-receptor on O2A progenitor cells in the developing rat brain. J Neurosci Res 1996;43:299-314
CrossRef | Web of Science | Medline14
Nishiyama A ,Lin XH ,Giese N ,Heldin CH ,Stallcup WB . Interaction between NG2 proteoglycan and PDGF α-receptor on O2A progenitor cells is required for optimal response to PDGF. J Neurosci Res 1996;43:315-330
CrossRef | Web of Science | Medline15
Armstrong RC ,Dorn HH ,Kufta CV ,Friedman E ,Dubois-Dalcq ME . Pre-oligodendrocytes from adult human CNS. J Neurosci 1992;12:1538-1547
Web of Science | Medline16
Chang A ,Nishiyama A ,Peterson J ,Prineas J ,Trapp BD . NG2-positive oligodendrocyte progenitor cells in adult human brain and multiple sclerosis lesions. J Neurosci 2000;20:6404-6412
Web of Science | Medline17
Gogate N ,Verma L ,Zhou JM , et al. Plasticity in the adult human oligodendrocyte lineage. J Neurosci 1994;14:4571-4587
Web of Science | Medline18
Scolding N ,Franklin R ,Stevens S ,Heldin C-H ,Compston A ,Newcombe J . Oligodendrocyte progenitors are present in the normal adult human CNS and in the lesions of multiple sclerosis. Brain 1998;121:2221-2228
CrossRef | Web of Science | Medline19
Wolswijk G . Chronic stage multiple sclerosis lesions contain a relatively quiescent population of oligodendrocyte precursor cells. J Neurosci 1998;18:601-609
Web of Science | Medline20
Raff MC ,Miller RH ,Noble M . A glial progenitor cell that develops in vitro into an astrocyte or an oligodendrocyte depending on culture medium. Nature 1983;303:390-396
CrossRef | Web of Science | Medline21
Ffrench-Constant C ,Raff MC . Proliferating bipotential glial progenitor cells in adult rat optic nerve. Nature 1986;319:499-502
CrossRef | Web of Science | Medline22
Wolswijk G ,Noble M . Identification of an adult-specific glial progenitor cell. Development 1989;105:387-400
Web of Science | Medline23
Shi J ,Marinovich A ,Barres BA . Purification and characterization of adult oligodendrocyte precursor cells from the rat optic nerve. J Neurosci 1998;18:4627-4636
Web of Science | Medline24
Trapp BD ,Nishiyama A ,Cheng D ,Macklin W . Differentiation and death of premyelinating oligodendrocytes in developing rodent brain. J Cell Biol 1997;137:459-468
CrossRef | Web of Science | Medline25
Barres BA ,Hart IK ,Coles HSR , et al. Cell death and control of cell survival in the oligodendrocyte lineage. Cell 1992;70:31-46
CrossRef | Web of Science | Medline26
Duncan ID ,Grever WE ,Zhang S-C . Repair of myelin disease: strategies and progress in animal models. Mol Med Today 1997;3:554-561
CrossRef | Medline27
Kurtzke JF . Rating neurologic impairment in multiple sclerosis: an Expanded Disability Status Scale (EDSS). Neurology 1983;33:1444-1452
Web of Science | Medline28
Pfeiffer SE ,Warrington AE ,Bansal R . The oligodendrocyte and its many cellular processes. Trends Cell Biol 1993;3:191-197
CrossRef | Medline29
Prineas JW ,Kwon EE ,Goldenberg PZ , et al. Multiple sclerosis: oligodendrocyte proliferation and differentiation in fresh lesions. Lab Invest 1989;61:489-503
Web of Science | Medline30
Lucchinetti C ,Bruck W ,Parisi J ,Scheithauer B ,Rodriguez M ,Lassmann H . Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination. Ann Neurol 2000;47:707-717
CrossRef | Web of Science | Medline31
Ozawa K ,Suchanek G ,Breitschopf H , et al. Patterns of oligodendroglia pathology in multiple sclerosis. Brain 1994;117:1311-1322
CrossRef | Web of Science | Medline32
Bruck W ,Schmied M ,Suchanek G , et al. Oligodendrocytes in the early course of multiple sclerosis. Ann Neurol 1994;35:65-73
CrossRef | Web of Science | Medline33
Wolswijk G . Oligodendrocyte survival, loss and birth in lesions of chronic-stage multiple sclerosis. Brain 2000;123:105-115
CrossRef | Web of Science | Medline34
Barres BA ,Jacobson MD ,Schmid R ,Sendtner M ,Raff MC . Does oligodendrocyte survival depend on axons? Curr Biol 1993;3:489-497
CrossRef | Web of Science | Medline35
Ueda H ,Levine JM ,Miller RH ,Trapp BD . Rat optic nerve oligodendrocytes develop in the absence of viable retinal ganglion cell axons. J Cell Biol 1999;146:1365-1374
CrossRef | Web of Science | Medline36
Jeffery ND ,Blakemore WF . Locomotor deficits induced by experimental spinal cord demyelination are abolished by spontaneous remyelination. Brain 1997;120:27-37
CrossRef | Web of Science | Medline37
Kornek B ,Storch MK ,Weissert R , et al. Multiple sclerosis and chronic autoimmune encephalomyelitis: a comparative quantitative study of axonal injury in active, inactive, and remyelinated lesions. Am J Pathol 2000;157:267-276
CrossRef | Web of Science | Medline38
Murray PD ,McGavern DB ,Sathornsumetee S ,Rodriguez M . Spontaneous remyelination following extensive demyelination is associated with improved neurological function in a viral model of multiple sclerosis. Brain 2001;124:1403-1416
CrossRef | Web of Science | Medline
- Citing Articles (205)
Citing Articles
1
Janusz J. Jadasz, Ludwig Aigner, Francisco J. Rivera, Patrick Küry. (2012) The remyelination Philosopher's Stone: stem and progenitor cell therapies for multiple sclerosis. Cell and Tissue Research
CrossRef2
Markus Kipp, Sandra Amor, Raphael Krauth, Cordian Beyer. (2012) Multiple sclerosis: neuroprotective alliance of estrogen-progesterone and gender. Frontiers in Neuroendocrinology
CrossRef3
Hui Fu, Santosh Kesari, Jun Cai. (2011) Tcf7l2 is Tightly Controlled During Myelin Formation. Cellular and Molecular Neurobiology
CrossRef4
H. Lassmann. (2011) Review: The architecture of inflammatory demyelinating lesions: implications for studies on pathogenesis. Neuropathology and Applied Neurobiology 37:7, 698-710
CrossRef5
M. Kipp, S. Gingele, F. Pott, T. Clarner, P. van der Valk, B. Denecke, L. Gan, V. Siffrin, F. Zipp, W. Dreher, W. Baumgartner, S. Pfeifenbring, R. Godbout, S. Amor, C. Beyer. (2011) BLBP-expression in astrocytes during experimental demyelination and in human multiple sclerosis lesions. Brain, Behavior, and Immunity 25:8, 1554-1568
CrossRef6
Diego C. Fernandez, Laura A. Pasquini, Damián Dorfman, Hernán J. Aldana Marcos, Ruth E. Rosenstein. (2011) Early Distal Axonopathy of the Visual Pathway in Experimental Diabetes. The American Journal of Pathology
CrossRef7
Catherine Fressinaud, Raphaël Berges, Joël Eyer. (2011) Axon cytoskeleton proteins specifically modulate oligodendrocyte growth and differentiation in vitro. Neurochemistry International
CrossRef8
Linda Ly, Michael H. Barnett, Yuan Z. Zheng, Twishi Gulati, John W. Prineas, Ben Crossett. (2011) Comprehensive Tissue Processing Strategy for Quantitative Proteomics of Formalin-fixed Multiple Sclerosis Lesions. Journal of Proteome Research 10:10, 4855-4868
CrossRef9
Emanuele Tirotta, Richard M. Ransohoff, Thomas E. Lane. (2011) CXCR2 signaling protects oligodendrocyte progenitor cells from IFN-γ/CXCL10-mediated apoptosis. Glia 59:10, 1518-1528
CrossRef10
Jeffrey K. Huang, Stephen P. J. Fancy, Chao Zhao, David H. Rowitch, Charles ffrench-Constant, Robin J. M. Franklin. (2011) Myelin Regeneration in Multiple Sclerosis: Targeting Endogenous Stem Cells. Neurotherapeutics 8:4, 650-658
CrossRef11
Tamir Ben-Hur. (2011) Cell Therapy for Multiple Sclerosis. Neurotherapeutics 8:4, 625-642
CrossRef12
Rebecca A. Sosa, Thomas G. Forsthuber. (2011) The Critical Role of Antigen-Presentation-Induced Cytokine Crosstalk in the Central Nervous System in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis. Journal of Interferon & Cytokine Research 31:10, 753-768
CrossRef13
Kazem Sharifi, Yusuke Morihiro, Motoko Maekawa, Yuki Yasumoto, Hisae Hoshi, Yasuhiro Adachi, Tomoo Sawada, Nobuko Tokuda, Hisatake Kondo, Takeo Yoshikawa, Michiyasu Suzuki, Yuji Owada. (2011) FABP7 expression in normal and stab-injured brain cortex and its role in astrocyte proliferation. Histochemistry and Cell Biology
CrossRef14
Nataly Urshansky, Karin Mausner-Fainberg, Eitan Auriel, Keren Regev, Arnon Karni. (2011) Low and dysregulated production of follistatin in immune cells of relapsing–remitting multiple sclerosis patients. Journal of Neuroimmunology 238:1-2, 96-103
CrossRef15
Francesco Girolamo, Giovanni Ferrara, Maurizio Strippoli, Marco Rizzi, Mariella Errede, Maria Trojano, Roberto Perris, Luisa Roncali, Maria Svelto, Tiziana Mennini, Daniela Virgintino. (2011) Cerebral cortex demyelination and oligodendrocyte precursor response to experimental autoimmune encephalomyelitis. Neurobiology of Disease 43:3, 678-689
CrossRef16
Hans Lassmann, Jack van Horssen. (2011) The molecular basis of neurodegeneration in multiple sclerosis. FEBS Letters
CrossRef17
Jingya Zhang, Elisabeth G. Kramer, Linnea Asp, Dipankar J. Dutta, Kristina Navrazhina, Trinh Pham, John N. Mariani, Azeb Tadesse Argaw, Carmen V. Melendez-Vasquez, Gareth R. John. (2011) Promoting myelin repair and return of function in multiple sclerosis. FEBS Letters
CrossRef18
Stephen P.J. Fancy, Jonah R. Chan, Sergio E. Baranzini, Robin J.M. Franklin, David H. Rowitch. (2011) Myelin Regeneration: A Recapitulation of Development?. Annual Review of Neuroscience 34:1, 21-43
CrossRef19
Brian Popko. (2011) Downregulating DR6 to drive remyelination. Nature Medicine 17:7, 779-780
CrossRef20
A. Defaux, M.-G. Zurich, P. Honegger, F. Monnet-Tschudi. (2011) Minocycline promotes remyelination in aggregating rat brain cell cultures after interferon-γ plus lipopolysaccharide-induced demyelination. Neuroscience 187, 84-92
CrossRef21
T. Clarner, A. Parabucki, C. Beyer, M. Kipp. (2011) Corticosteroids Impair Remyelination in the Corpus Callosum of Cuprizone-Treated Mice. Journal of Neuroendocrinology 23:7, 601-611
CrossRef22
M. R. Kotter, C. Stadelmann, H.-P. Hartung. (2011) Enhancing remyelination in disease--can we wrap it up?. Brain 134:7, 1882-1900
CrossRef23
Stephen P J Fancy, Emily P Harrington, Tracy J Yuen, John C Silbereis, Chao Zhao, Sergio E Baranzini, Charlotte C Bruce, Jose J Otero, Eric J Huang, Roel Nusse, Robin J M Franklin, David H Rowitch. (2011) Axin2 as regulatory and therapeutic target in newborn brain injury and remyelination. Nature Neuroscience 14:8, 1009-1016
CrossRef24
Ahmad Othman, David M. Frim, Paul Polak, Snezana Vujicic, Barry G. W. Arnason, Anne I. Boullerne. (2011) Olig1 is expressed in human oligodendrocytes during maturation and regeneration. Glia 59:6, 914-926
CrossRef25
Zhida Su, Yimin Yuan, Jingjing Chen, Yanling Zhu, Yang Qiu, Feng Zhu, Aijun Huang, Cheng He. (2011) Reactive Astrocytes Inhibit the Survival and Differentiation of Oligodendrocyte Precursor Cells by Secreted TNF-α. Journal of Neurotrauma 28:6, 1089-1100
CrossRef26
Sabah Mozafari, Mohammad Javan, Mohammad Amin Sherafat, Javad Mirnajafi-Zadeh, Motahareh Heibatollahi, Shahram Pour-Beiranvand, Taki Tiraihi, Abolhasan Ahmadiani. (2011) Analysis of Structural and Molecular Events Associated with Adult Rat Optic Chiasm and Nerves Demyelination and Remyelination; Possible Role for 3rd Ventricle Proliferating Cells. NeuroMolecular Medicine 13:2, 138-150
CrossRef27
Jianmei Ma, Kenji F. Tanaka, Takahiro Shimizu, Claude C.A. Bernard, Akiyoshi Kakita, Hitoshi Takahashi, Steven E. Pfeiffer, Kazuhiro Ikenaka. (2011) Microglial cystatin F expression is a sensitive indicator for ongoing demyelination with concurrent remyelination. Journal of Neuroscience Research 89:5, 639-649
CrossRef28
Jeffrey A. Cohen, Jerold Chun. (2011) Mechanisms of fingolimod's efficacy and adverse effects in multiple sclerosis. Annals of Neurology 69:5, 759-777
CrossRef29
C. Caillava, R. Vandenbosch, B. Jablonska, C. Deboux, G. Spigoni, V. Gallo, B. Malgrange, A. Baron-Van Evercooren. (2011) Cdk2 loss accelerates precursor differentiation and remyelination in the adult central nervous system. The Journal of Cell Biology 193:2, 397-407
CrossRef30
G. Piaton, M.-S. Aigrot, A. Williams, S. Moyon, V. Tepavcevic, I. Moutkine, J. Gras, K. S. Matho, A. Schmitt, H. Soellner, A. B. Huber, P. Ravassard, C. Lubetzki. (2011) Class 3 semaphorins influence oligodendrocyte precursor recruitment and remyelination in adult central nervous system. Brain 134:4, 1156-1167
CrossRef31
David Kremer, Orhan Aktas, Hans-Peter Hartung, Patrick Küry. (2011) The complex world of oligodendroglial differentiation inhibitors. Annals of Neurology 69:4, 602-618
CrossRef32
L. S. Laursen, C. W. Chan, C. ffrench-Constant. (2011) Translation of myelin basic protein mRNA in oligodendrocytes is regulated by integrin activation and hnRNP-K. The Journal of Cell Biology 192:5, 797-811
CrossRef33
Nataly Urshansky, Karin Mausner-Fainberg, Eitan Auriel, Keren Regev, Natan M. Bornstein, Arnon Karni. (2011) Reduced production of noggin by immune cells of patients with relapsing–remitting multiple sclerosis. Journal of Neuroimmunology 232:1-2, 171-178
CrossRef34
Jingya Zhang, Elisabeth G. Kramer, Sean Mahase, Dipankar J. Dutta, Virginie Bonnamain, Azeb T. Argaw, Gareth R. John. (2011) Targeting Oligodendrocyte Protection and Remyelination in Multiple Sclerosis. Mount Sinai Journal of Medicine: A Journal of Translational and Personalized Medicine 78:2, 244-257
CrossRef35
Khalid A. Hanafy, Jacob A. Sloane. (2011) Regulation of remyelination in multiple sclerosis. FEBS Letters
CrossRef36
Veronique E. Miron, Tanja Kuhlmann, Jack P. Antel. (2011) Cells of the oligodendroglial lineage, myelination, and remyelination. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1812:2, 184-193
CrossRef37
Jeffrey K. Huang, Robin J.M. Franklin. (2011) Regenerative medicine in multiple sclerosis: Identifying pharmacological targets of adult neural stem cell differentiation. Neurochemistry International
CrossRef38
Jeffrey A. Cohen. (2011) Multiple Sclerosis: New Insights in Pathogenesis and Novel Therapeutics. Annual Review of Medicine 63:1, 110301100719093
CrossRef39
Nanako Sato, Chika Seiwa, Michihiro Uruse, Masahiro Yamamoto, Kayoko Tanaka, Takuya Kawakita, Yasuhiro Komatsu, Akio Yasukawa, Masakatsu Takao, Chiaki Kudo, Atsuhiko Hasegawa, Atushi Ishige, Kenji Watanabe, Hiroaki Asou. (2011) Administration of Chinpi, a Component of the Herbal Medicine Ninjin-Youei-To, Reverses Age-Induced Demyelination. Evidence-Based Complementary and Alternative Medicine 2011, 1-9
CrossRef40
Andreas Junker, Reinhard Hohlfeld, Edgar Meinl. (2011) The emerging role of microRNAs in multiple sclerosis. Nature Reviews Neurology 7:1, 56-59
CrossRef41
Jeffrey K Huang, Andrew A Jarjour, Brahim Nait Oumesmar, Christophe Kerninon, Anna Williams, Wojciech Krezel, Hiroyuki Kagechika, Julien Bauer, Chao Zhao, Anne Baron-Van Evercooren, Pierre Chambon, Charles ffrench-Constant, Robin J M Franklin. (2011) Retinoid X receptor gamma signaling accelerates CNS remyelination. Nature Neuroscience 14:1, 45-53
CrossRef42
Ilka Imbschweiler, Frauke Seehusen, Claas-Tido Peck, Mohamed Omar, Wolfgang Baumgärtner, Konstantin Wewetzer. (2011) Increased p75 neurotrophin receptor expression in the canine distemper virus model of multiple sclerosis identifies aldynoglial schwann cells that emerge in response to axonal damage. Glian/a-n/a
CrossRef43
Peter Göttle, David Kremer, Sebastian Jander, Veysel Ödemis, Jürgen Engele, Hans-Peter Hartung, Patrick Küry. (2010) Activation of CXCR7 receptor promotes oligodendroglial cell maturation. Annals of Neurology 68:6, 915-924
CrossRef44
Romana Höftberger, Stephanie Fink, Fahmy Aboul-Enein, Gergö Botond, Judit Olah, Timea Berki, Judit Ovadi, Hans Lassmann, Herbert Budka, Gabor G. Kovacs. (2010) Tubulin polymerization promoting protein (TPPP/p25) as a marker for oligodendroglial changes in multiple sclerosis. Glia 58:15, 1847-1857
CrossRef45
Iryna Ziabreva, Graham Campbell, Julia Rist, Jessica Zambonin, Joanna Rorbach, Mateusz M. Wydro, Hans Lassmann, Robin J. M. Franklin, Don Mahad. (2010) Injury and differentiation following inhibition of mitochondrial respiratory chain complex IV in rat oligodendrocytes. Glia 58:15, 1827-1837
CrossRef46
David H. Rowitch, Arnold R. Kriegstein. (2010) Developmental genetics of vertebrate glial–cell specification. Nature 468:7321, 214-222
CrossRef47
Ajaib S. Paintlia, Manjeet K. Paintlia, Avtar K. Singh, John K. Orak, Inderjit Singh. (2010) Activation of PPAR-γ and PTEN cascade participates in lovastatin-mediated accelerated differentiation of oligodendrocyte progenitor cells. Glia 58:14, 1669-1685
CrossRef48
D. K. Crawford, M. Mangiardi, B. Song, R. Patel, S. Du, M. V. Sofroniew, R. R. Voskuhl, S. K. Tiwari-Woodruff. (2010) Oestrogen receptor ligand: a novel treatment to enhance endogenous functional remyelination. Brain 133:10, 2999-3016
CrossRef49
Stephen P.J. Fancy, Mark R. Kotter, Emily P. Harrington, Jeffrey K. Huang, Chao Zhao, David H. Rowitch, Robin J.M. Franklin. (2010) Overcoming remyelination failure in multiple sclerosis and other myelin disorders. Experimental Neurology 225:1, 18-23
CrossRef50
J. A. Sloane, C. Batt, Y. Ma, Z. M. Harris, B. Trapp, T. Vartanian. (2010) Hyaluronan blocks oligodendrocyte progenitor maturation and remyelination through TLR2. Proceedings of the National Academy of Sciences 107:25, 11555-11560
CrossRef51
Gabrièle Piaton, Robert M. Gould, Catherine Lubetzki. (2010) Axon-oligodendrocyte interactions during developmental myelination, demyelination and repair. Journal of Neurochemistryno-no
CrossRef52
Hong-jun Yu, Jun Fei, Xing-shu Chen, Qi-yan Cai, Hong-liang Liu, Guo-dong Liu, Zhong-xiang Yao. (2010) Progesterone attenuates neurological behavioral deficits of experimental autoimmune encephalomyelitis through remyelination with nucleus-sublocalized Olig1 protein. Neuroscience Letters 476:1, 42-45
CrossRef53
Giuseppe Scalabrino, Daniela Galimberti, Elena Mutti, Diego Scalabrini, Daniela Veber, Milena De Riz, Fabrizia Bamonti, Elisabetta Capello, Giovanni Luigi Mancardi, Elio Scarpini. (2010) Loss of epidermal growth factor regulation by cobalamin in multiple sclerosis. Brain Research 1333, 64-71
CrossRef54
Daniel Chesik, Jacques De Keyser, Reinier Bron, Gwenny M. Fuhler. (2010) Insulin-like growth factor binding protein-1 activates integrin-mediated intracellular signaling and migration in oligodendrocytes. Journal of Neurochemistry
CrossRef55
Orhan Aktas, Bernd Kieseier, Hans-Peter Hartung. (2010) Neuroprotection, regeneration and immunomodulation: broadening the therapeutic repertoire in multiple sclerosis. Trends in Neurosciences 33:3, 140-152
CrossRef56
Jens Watzlawik, Arthur E Warrington, Moses Rodriguez. (2010) Importance of oligodendrocyte protection, BBB breakdown and inflammation for remyelination. Expert Review of Neurotherapeutics 10:3, 441-457
CrossRef57
Nobukazu Miyamoto, Ryota Tanaka, Hideki Shimura, Terubumi Watanabe, Hideo Mori, Masafumi Onodera, Hideki Mochizuki, Nobutaka Hattori, Takao Urabe. (2010) Phosphodiesterase III inhibition promotes differentiation and survival of oligodendrocyte progenitors and enhances regeneration of ischemic white matter lesions in the adult mammalian brain. Journal of Cerebral Blood Flow & Metabolism 30:2, 299-310
CrossRef58
Monika Bradl, Hans Lassmann. (2010) Oligodendrocytes: biology and pathology. Acta Neuropathologica 119:1, 37-53
CrossRef59
Clare E. Buckley, Anita Marguerie, Wendy K. Alderton, Robin J. M. Franklin. (2010) Temporal dynamics of myelination in the zebrafish spinal cord. GliaNA-NA
CrossRef60
D.K. Crawford, M. Mangiardi, X. Xia, H.E. López-Valdés, S.K. Tiwari-Woodruff. (2009) Functional recovery of callosal axons following demyelination: a critical window. Neuroscience 164:4, 1407-1421
CrossRef61
Markus Kipp, Tim Clarner, Jon Dang, Sjef Copray, Cordian Beyer. (2009) The cuprizone animal model: new insights into an old story. Acta Neuropathologica 118:6, 723-736
CrossRef62
Audrey D. Forrest, Hilary E. Beggs, Louis F. Reichardt, Jeffrey L. Dupree, Raymond J. Colello, Babette Fuss. (2009) Focal adhesion kinase (FAK): A regulator of CNS myelination. Journal of Neuroscience Research 87:15, 3456-3464
CrossRef63
Susan M. Staugaitis, Bruce D. Trapp. (2009) NG2-positive glia in the human central nervous system. Neuron Glia Biology 5:3-4, 35
CrossRef64
Ying Chen, Heng Wu, Shuzong Wang, Hisami Koito, Jianrong Li, Feng Ye, Jenny Hoang, Sabine S Escobar, Alexander Gow, Heather A Arnett, Bruce D Trapp, Nitin J Karandikar, Jenny Hsieh, Q Richard Lu. (2009) The oligodendrocyte-specific G protein–coupled receptor GPR17 is a cell-intrinsic timer of myelination. Nature Neuroscience 12:11, 1398-1406
CrossRef65
T. Kuhlmann, T. Goldschmidt, J. Antel, C. Wegner, F. König, I. Metz, W. Brück. (2009) Gender differences in the histopathology of MS?. Journal of the Neurological Sciences 286:1-2, 86-91
CrossRef66
Maya N. Hatch, Chris S. Schaumburg, Thomas E. Lane, Hans S. Keirstead. (2009) Endogenous remyelination is induced by transplant rejection in a viral model of multiple sclerosis. Journal of Neuroimmunology 212:1-2, 74-81
CrossRef67
J. Camara, Z. Wang, C. Nunes-Fonseca, H. C. Friedman, M. Grove, D. L. Sherman, N. H. Komiyama, S. G. Grant, P. J. Brophy, A. Peterson, C. ffrench-Constant. (2009) Integrin-mediated axoglial interactions initiate myelination in the central nervous system. The Journal of Cell Biology 185:4, 699-712
CrossRef68
Neus Franco-Pons, Jordi Tomàs, Bárbara Roig, Carme Auladell, Lourdes Martorell, Elisabet Vilella. (2009) Discoidin Domain Receptor 1, a Tyrosine Kinase Receptor, is Upregulated in an Experimental Model of Remyelination and During Oligodendrocyte Differentiation In Vitro. Journal of Molecular Neuroscience 38:1, 2-11
CrossRef69
Maren Lindner, Jantje Fokuhl, Franziska Linsmeier, Corinna Trebst, Martin Stangel. (2009) Chronic toxic demyelination in the central nervous system leads to axonal damage despite remyelination
. Neuroscience Letters 453:2, 120-125
CrossRef70
Sha Mi, Robert H. Miller, Wei Tang, Xinhua Lee, Bing Hu, Wutain Wu, Yiping Zhang, Christopher B. Shields, Yongjie Zhang, Steven Miklasz, Diana Shea, Jeff Mason, Robin J. M. Franklin, Benxiu Ji, Zhaohui Shao, Alain Chédotal, Frederic Bernard, Aude Roulois, Janfeng Xu, Vincent Jung, Blake Pepinsky. (2009) Promotion of central nervous system remyelination by induced differentiation of oligodendrocyte precursor cells. Annals of Neurology 65:3, 304-315
CrossRef71
Jeffrey A. Cohen. (2009) The future of multiple sclerosis treatment. Journal of the Neurological Sciences 277, S55-S61
CrossRef72
Akiko Nishiyama, Mila Komitova, Ryusuke Suzuki, Xiaoqin Zhu. (2009) Polydendrocytes (NG2 cells): multifunctional cells with lineage plasticity. Nature Reviews Neuroscience 10:1, 9-22
CrossRef73
Jin Nakahara, Kohsuke Kanekura, Mikiro Nawa, Sadakazu Aiso, Norihiro Suzuki. (2008) Abnormal expression of TIP30 and arrested nucleocytoplasmic transport within oligodendrocyte precursor cells in multiple sclerosis. Journal of Clinical Investigation
CrossRef74
Robin J. M. Franklin, Charles ffrench-Constant. (2008) Remyelination in the CNS: from biology to therapy. Nature Reviews Neuroscience 9:11, 839-855
CrossRef75
Heidi Snethen, Seth Love, Neil Scolding. (2008) Disease-responsive neural precursor cells are present in multiple sclerosis lesions. Regenerative Medicine 3:6, 835-847
CrossRef76
Richard A Rudick, Sha Mi, Alfred W Sandrock. (2008) LINGO-1 antagonists as therapy for multiple sclerosis: in vitro and in vivo evidence. Expert Opinion on Biological Therapy 8:10, 1561-1570
CrossRef77
Alastair Compston, Alasdair Coles. (2008) Multiple sclerosis. The Lancet 372:9648, 1502-1517
CrossRef78
Yue Wang, Jaime Imitola, Stine Rasmussen, Kevin C. O'Connor, Samia J. Khoury. (2008) Paradoxical dysregulation of the neural stem cell pathway sonic hedgehog-gli1 in autoimmune encephalomyelitis and multiple sclerosis. Annals of Neurology 64:4, 417-427
CrossRef79
Tamir Ben-Hur, Steven A. Goldman. (2008) Prospects of Cell Therapy for Disorders of Myelin. Annals of the New York Academy of Sciences 1142:1, 218-249
CrossRef80
Siming Shen, Juan Sandoval, Victoria A Swiss, Jiadong Li, Jeff Dupree, Robin J M Franklin, Patrizia Casaccia-Bonnefil. (2008) Age-dependent epigenetic control of differentiation inhibitors is critical for remyelination efficiency. Nature Neuroscience 11:9, 1024-1034
CrossRef81
Carlos E. Pedraza, Raymond Monk, Junying Lei, Qi Hao, Wendy B. Macklin. (2008) Production, characterization, and efficient transfection of highly pure oligodendrocyte precursor cultures from mouse embryonic neural progenitors. Glia 56:12, 1339-1352
CrossRef82
Xiaoming Gong, Tong Lin, Zhaohui Sun, Min Fu, Huancong Zuo, Zuoping Xie. (2008) Olig1 is downregulated in oligodendrocyte progenitor cell differentiation. NeuroReport 19:12, 1203-1207
CrossRef83
T. Kuhlmann, V. Miron, Q. Cuo, C. Wegner, J. Antel, W. Bruck. (2008) Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis. Brain 131:7, 1749-1758
CrossRef84
Nadine Wilczak, Daniel Chesik, Dick Hoekstra, Jacques De Keyser. (2008) IGF binding protein alterations on periplaque oligodendrocytes in multiple sclerosis: Implications for remyelination. Neurochemistry International 52:8, 1431-1435
CrossRef85
Elizabeth A. Young, Christie D. Fowler, Grahame J. Kidd, Ansi Chang, Richard Rudick, Elizabeth Fisher, Bruce D. Trapp. (2008) Imaging correlates of decreased axonal Na + /K + ATPase in chronic multiple sclerosis lesions. Annals of Neurology 63:4, 428-435
CrossRef86
Shucui Jiang, Patrizia Ballerini, Silvana Buccella, Patricia Giuliani, Cai Jiang, Xinjie Huang, Michel P. Rathbone. (2008) Remyelination after chronic spinal cord injury is associated with proliferation of endogenous adult progenitor cells after systemic administration of guanosine. Purinergic Signalling 4:1, 61-71
CrossRef87
Silva Markovic-Plese, Avtar K Singh, Inderjit Singh. (2008) Therapeutic potential of statins in multiple sclerosis: immune modulation, neuroprotection and neurorepair. Future Neurology 3:2, 153-167
CrossRef88
Yasir A. Syed, Alexandra S. Baer, Gert Lubec, Harald Hoeger, Georg Widhalm, Mark R. Kotter. (2008) Inhibition of oligodendrocyte precursor cell differentiation by myelin-associated proteins. Neurosurgical FOCUS 24:3-4, E5
CrossRef89
Robin J. M. Franklin, Mark R. Kotter. (2008) The biology of CNS remyelination. Journal of Neurology 255:S1, 19-25
CrossRef90
Teresa G. D'Aversa, Eliseo A. Eugenin, Joan W. Berman. (2008) CD40-CD40 ligand interactions in human microglia induce CXCL8 (interleukin-8) secretion by a mechanism dependent on activation of ERK1/2 and nuclear translocation of nuclear factor-κB (NFκB) and activator protein-1 (AP-1). Journal of Neuroscience Research 86:3, 630-639
CrossRef91
Maciej Jurynczyk, Anna Jurewicz, Bartosz Bielecki, Cedric S. Raine, Krzysztof Selmaj. (2008) Overcoming failure to repair demyelination in EAE: γ-secretase inhibition of Notch signaling. Journal of the Neurological Sciences 265:1-2, 5-11
CrossRef92
W.F. Blakemore, K-A. Irvine. (2008) Endogenous or exogenous oligodendrocytes for remyelination. Journal of the Neurological Sciences 265:1-2, 43-46
CrossRef93
Niklas K. U. Koehler, Markus Roebbert, Kourosh Dehghani, Matthias Ballmaier, Peter Claus, Stephan von Hoersten, Mona Shing, Per Odin, Jürgen Strehlau, Fedor Heidenreich. (2008) Up-regulation of platelet-derived growth factor by peripheral-blood leukocytes during experimental allergic encephalomyelitis. Journal of Neuroscience Research 86:2, 392-402
CrossRef94
W.F. Blakemore. (2008) Regeneration and repair in multiple sclerosis: The view of experimental pathology. Journal of the Neurological Sciences 265:1-2, 1-4
CrossRef95
Tamara Glaser, Tanja Schmandt, Oliver Brüstle. (2008) Generation and potential biomedical applications of embryonic stem cell-derived glial precursors. Journal of the Neurological Sciences 265:1-2, 47-58
CrossRef96
Ian D. Duncan. (2008) Replacing cells in multiple sclerosis. Journal of the Neurological Sciences 265:1-2, 89-92
CrossRef97
S. Chandran, D. Hunt, A. Joannides, C. Zhao, A. Compston, R. J.M Franklin. (2008) Myelin repair: the role of stem and precursor cells in multiple sclerosis. Philosophical Transactions of the Royal Society B: Biological Sciences 363:1489, 171-183
CrossRef98
Sha Mi, Alfred Sandrock, Robert H. Miller. (2008) LINGO-1 and its role in CNS repair. The International Journal of Biochemistry & Cell Biology 40:10, 1971-1978
CrossRef99
Radmila Filipovic, Nada Zecevic. (2008) The effect of CXCL1 on human fetal oligodendrocyte progenitor cells. Glia 56:1, 1-15
CrossRef100
Til Menge, Martin S Weber, Bernhard Hemmer, Bernd C Kieseier, Hans-Christian von Büdingen, Clemens Warnke, Scott S Zamvil, Aaron Boster, Omar Khan, Hans-Peter Hartung, Olaf Stüve. (2008) Disease-Modifying Agents for Multiple Sclerosis. Drugs 68:17, 2445-2468
CrossRef101
Xiaoxin Cheng, Yaping Wang, Qian He, Mengsheng Qiu, Scott R. Whittemore, Qilin Cao. (2007) Bone Morphogenetic Protein Signaling and Olig1/2 Interact to Regulate the Differentiation and Maturation of Adult Oligodendrocyte Precursor Cells. Stem Cells 25:12, 3204-3214
CrossRef102
Robert H Miller, Sha Mi. (2007) Dissecting demyelination. Nature Neuroscience 10:11, 1351-1354
CrossRef103
Stella Elkabes, Hong Li. (2007) Proteomic strategies in multiple sclerosis and its animal models. PROTEOMICS – CLINICAL APPLICATIONS 1:11, 1393-1405
CrossRef104
Regina C Armstrong. (2007) Growth factor regulation of remyelination: behind the growing interest in endogenous cell repair of the CNS. Future Neurology 2:6, 689-697
CrossRef105
Adam C. Vana, Nicole C. Flint, Norah E. Harwood, Tuan Q. Le, Marcus Fruttiger, Regina C. Armstrong. (2007) Platelet-Derived Growth Factor Promotes Repair of Chronically Demyelinated White Matter. Journal of Neuropathology and Experimental Neurology 66:11, 975-988
CrossRef106
M. Lindner, S. Heine, K. Haastert, N. Garde, J. Fokuhl, F. Linsmeier, C. Grothe, W. Baumgärtner, M. Stangel. (2007) Sequential myelin protein expression during remyelination reveals fast and efficient repair after central nervous system demyelination. Neuropathology and Applied Neurobiology 0:0, 071026235340007-???
CrossRef107
Paolo A. Muraro, Bibiana Bielekova. (2007) Emerging therapies for multiple sclerosis. Neurotherapeutics 4:4, 676-692
CrossRef108
Jason Sharp, Hans S Keirstead. (2007) Therapeutic applications of oligodendrocyte precursors derived from human embryonic stem cells. Current Opinion in Biotechnology 18:5, 434-440
CrossRef109
Reaz Vawda, Jennifer Woodbury, Matthew Covey, Steven W. Levison, Huseyin Mehmet. (2007) Stem cell therapies for perinatal brain injuries. Seminars in Fetal and Neonatal Medicine 12:4, 259-272
CrossRef110
J. E. Simpson, M. S. Fernando, L. Clark, P. G. Ince, F. Matthews, G. Forster, J. T. O'Brien, R. Barber, R. N. Kalaria, C. Brayne, P. J. Shaw, C. E. Lewis, S. B. Wharton, . (2007) White matter lesions in an unselected cohort of the elderly: astrocytic, microglial and oligodendrocyte precursor cell responses. Neuropathology and Applied Neurobiology 33:4, 410-419
CrossRef111
Eva Herrero-Herranz, Luis A. Pardo, Gertrude Bunt, Ralf Gold, Walter Stühmer, Ralf A. Linker. (2007) Re-Expression of a Developmentally Restricted Potassium Channel in Autoimmune Demyelination. The American Journal of Pathology 171:2, 589-598
CrossRef112
Karen L. Baracskay, Grahame J. Kidd, Robert H. Miller, Bruce D. Trapp. (2007) NG2-positive cells generate A2B5-positive oligodendrocyte precursor cells. Glia 55:10, 1001-1010
CrossRef113
Jeffrey I. Greenstein. (2007) Current concepts of the cellular and molecular pathophysiology of multiple sclerosis. Developmental Neurobiology 67:9, 1248-1265
CrossRef114
C. Kleinschnitz, S.G. Meuth, B.C. Kieseier, H. Wiendl. (2007) Multiple-Sklerose-Update zur Pathophysiologie und neuen immuntherapeutischen Ansätzen. Der Nervenarzt 78:8, 883-911
CrossRef115
Simon Fillatreau, Stephen M Anderton. (2007) B-cell function in CNS inflammatory demyelinating disease: a complexity of roles and a wealth of possibilities. Expert Review of Clinical Immunology 3:4, 565-578
CrossRef116
R. Patani, M. Balaratnam, A. Vora, R. Reynolds. (2007) Remyelination can be extensive in multiple sclerosis despite a long disease course. Neuropathology and Applied Neurobiology 33:3, 277-287
CrossRef117
Jessica Carmen, Tim Magnus, Riccardo Cassiani-Ingoni, Larry Sherman, Mahendra S. Rao, Mark P. Mattson. (2007) Revisiting the astrocyte–oligodendrocyte relationship in the adult CNS. Progress in Neurobiology 82:3, 151-162
CrossRef118
Adam C. Vana, Claudia F. Lucchinetti, Tuan Q. Le, Regina C. Armstrong. (2007) Myelin transcription factor 1 (Myt1) expression in demyelinated lesions of rodent and human CNS. Glia 55:7, 687-697
CrossRef119
Zhen Wang, Holly Colognato, Charles ffrench-Constant. (2007) Contrasting effects of mitogenic growth factors on myelination in neuron–oligodendrocyte co-cultures. Glia 55:5, 537-545
CrossRef120
Moses Rodriguez. (2007) Effectors of Demyelination and Remyelination in the CNS: Implications for Multiple Sclerosis. Brain Pathology 17:2, 219-229
CrossRef121
Monika Albert, Jack Antel, Wolfgang Brück, Christine Stadelmann. (2007) Extensive Cortical Remyelination in Patients with Chronic Multiple Sclerosis. Brain Pathology 17:2, 129-138
CrossRef122
Arthur E. Warrington, Allan J. Bieber, Bogoljub Ciric, Larry R. Pease, Virginia Van Keulen, Moses Rodriguez. (2007) A recombinant human IgM promotes myelin repair after a single, very low dose. Journal of Neuroscience Research 85:5, 967-976
CrossRef123
Chika Seiwa, Masahiro Yamamoto, Kayoko Tanaka, Masato Fukutake, Toshiyuki Ueki, Shuichi Takeda, Risa Sakai, Atsushi Ishige, Kenji Watanabe, Masumi Akita, Takeshi Yagi, Kotaro Tanaka, Hiroaki Asou. (2007) Restoration of FcRγ/Fyn signaling repairs central nervous system demyelination. Journal of Neuroscience Research 85:5, 954-966
CrossRef124
Shalini Kumar, Juan Carlos Biancotti, Masahiro Yamaguchi, Jean Vellis. (2007) Combination of Growth Factors Enhances Remyelination in a Cuprizone-induced Demyelination Mouse Model. Neurochemical Research 32:4-5, 783-797
CrossRef125
B. Nait-Oumesmar, N. Picard-Riera, C. Kerninon, L. Decker, D. Seilhean, G. U. Hoglinger, E. C. Hirsch, R. Reynolds, A. Baron-Van Evercooren. (2007) Activation of the subventricular zone in multiple sclerosis: Evidence for early glial progenitors. Proceedings of the National Academy of Sciences 104:11, 4694-4699
CrossRef126
Jason F. Talbott, Qilin Cao, James Bertram, Michael Nkansah, Richard L. Benton, Erin Lavik, Scott R. Whittemore. (2007) CNTF promotes the survival and differentiation of adult spinal cord-derived oligodendrocyte precursor cells in vitro but fails to promote remyelination in vivo. Experimental Neurology 204:1, 485-489
CrossRef127
Sean J. Pittock, Claudia F. Lucchinetti. (2007) The Pathology of MS. The Neurologist 13:2, 45-56
CrossRef128
Phillip J. Albrecht, Jonathan C. Enterline, Jason Cromer, Steven W. Levison. (2007) CNTF-Activated Astrocytes Release a Soluble Trophic Activity for Oligodendrocyte Progenitors. Neurochemical Research 32:2, 263-271
CrossRef129
Joana Câmara, Charles ffrench-Constant. (2007) Lessons from oligodendrocyte biology on promoting repair in multiple sclerosis. Journal of Neurology 254:S1, I15-I22
CrossRef130
Thomas Seifert, Jan Bauer, Robert Weissert, Franz Fazekas, Maria K. Storch. (2007) Notch1 and its ligand Jagged1 are present in remyelination in a T-cell- and antibody-mediated model of inflammatory demyelination. Acta Neuropathologica 113:2, 195-203
CrossRef131
Brandon B Kirby, Norio Takada, Andrew J Latimer, Jimann Shin, Thomas J Carney, Robert N Kelsh, Bruce Appel. (2006) In vivo time-lapse imaging shows dynamic oligodendrocyte progenitor behavior during zebrafish development. Nature Neuroscience 9:12, 1506-1511
CrossRef132
Yong-Xing Zhou, Nicole C. Flint, Joshua C. Murtie, Tuan Q. Le, Regina C. Armstrong. (2006) Retroviral lineage analysis of fibroblast growth factor receptor signaling in FGF2 inhibition of oligodendrocyte progenitor differentiation. Glia 54:6, 578-590
CrossRef133
Chao Zhao, Wen-Wu Li, Robin J.M. Franklin. (2006) Differences in the early inflammatory responses to toxin-induced demyelination are associated with the age-related decline in CNS remyelination. Neurobiology of Aging 27:9, 1298-1307
CrossRef134
Anna Setzu, Justin D. Lathia, Chao Zhao, Karen Wells, Mahendra S. Rao, Charles ffrench-Constant, Robin J. M. Franklin. (2006) Inflammation stimulates myelination by transplanted oligodendrocyte precursor cells. Glia 54:4, 297-303
CrossRef135
E KAMALISARVESTANI, A NIKSERESHT, M ALIPARASTI, M VESSAL. (2006) IL-8 (−251 A/T) and CXCR2 (+1208 C/T) gene polymorphisms and risk of multiple sclerosis in Iranian patients. Neuroscience Letters 404:1-2, 159-162
CrossRef136
Helle H. Nielsen, Rune Ladeby, Nina Drøjdahl, Alan C. Peterson, Bente Finsen. (2006) Axonal degeneration stimulates the formation of NG2+ cells and oligodendrocytes in the mouse. Glia 54:2, 105-115
CrossRef137
Heather C. Wilson, Neil J. Scolding, Cedric S. Raine. (2006) Co-expression of PDGF α receptor and NG2 by oligodendrocyte precursors in human CNS and multiple sclerosis lesions. Journal of Neuroimmunology 176:1-2, 162-173
CrossRef138
Keith L. Ligon, Stephen P.J. Fancy, Robin J.M. Franklin, David H. Rowitch. (2006) Olig gene function in CNS development and disease. Glia 54:1, 1-10
CrossRef139
Jin Nakahara, Sadakazu Aiso. (2006) Fc Receptor-Positive Cells in Remyelinating Multiple Sclerosis Lesions. Journal of Neuropathology and Experimental Neurology 65:6, 582-591
CrossRef140
Anne I. Boullerne, Joyce A. Benjamins. (2006) Nitric Oxide Synthase Expression and Nitric Oxide Toxicity in Oligodendrocytes. Antioxidants & Redox Signaling 8:5-6, 967-980
CrossRef141
Martin Stangel, Corinna Trebst. (2006) Remyelination strategies: New advancements toward a regenerative treatment in multiple sclerosis. Current Neurology and Neuroscience Reports 6:3, 229-235
CrossRef142
Michael A. Fox, Fatemah S. Afshari, John K. Alexander, Raymond J. Colello, Babette Fuss. (2006) Growth conelike sensorimotor structures are characteristic features of postmigratory, premyelinating oligodendrocytes. Glia 53:5, 563-566
CrossRef143
Laurent Nguyen, Laurence Borgs, Renaud Vandenbosch, Jean-Marie Mangin, Pierre Beukelaers, Gustave Moonen, Vittorio Gallo, Brigitte Malgrange, Shibeshih Belachew. (2006) TheYin andYang of cell cycle progression and differentiation in the oligodendroglial lineage. Mental Retardation and Developmental Disabilities Research Reviews 12:2, 85-96
CrossRef144
Qi-Dong Hu, Quan-Hong Ma, Gianfranco Gennarini, Zhi-Cheng Xiao. (2006) Cross-Talk between F3/Contactin and Notch at Axoglial Interface: A Role in Oligodendrocyte Development. Developmental Neuroscience 28:1-2, 25-33
CrossRef145
Ralf Gold. (2005) Overcoming failure to repair demyelination in EAE: An important step towards neuroprotection in multiple sclerosis. Journal of Neuroimmunology 170:1-2, 1-2
CrossRef146
Maciej Jurynczyk, Anna Jurewicz, Bartosz Bielecki, Cedric S. Raine, Krzysztof Selmaj. (2005) Inhibition of Notch signaling enhances tissue repair in an animal model of multiple sclerosis. Journal of Neuroimmunology 170:1-2, 3-10
CrossRef147
Silvia Marconi, Luca De Toni, Laura Lovato, Elisa Tedeschi, Luigi Gaetti, Michele Acler, Bruno Bonetti. (2005) Expression of gangliosides on glial and neuronal cells in normal and pathological adult human brain. Journal of Neuroimmunology 170:1-2, 115-121
CrossRef148
Hans S. Keirstead. (2005) Stem cells for the treatment of myelin loss. Trends in Neurosciences 28:12, 677-683
CrossRef149
Li-Jin Chew, William C. King, Ann Kennedy, Vittorio Gallo. (2005) Interferon-γ inhibits cell cycle exit in differentiating oligodendrocyte progenitor cells. Glia 52:2, 127-143
CrossRef150
Cristina Cid, Jose C. Alvarez-Cermeno, Matilde Salinas, Alberto Alcazar. (2005) Anti-heat shock protein 90β antibodies decrease pre-oligodendrocyte population in perinatal and adult cell cultures. Implications for remyelination in multiple sclerosis. Journal of Neurochemistry 95:2, 349-360
CrossRef151
P.S. Piraino, T.A. Yednock, E.K. Messersmith, M.A. Pleiss, S.B. Freedman, R.R. Hammond, S.J. Karlik. (2005) Spontaneous remyelination following prolonged inhibition of α4 integrin in chronic EAE. Journal of Neuroimmunology 167:1-2, 53-63
CrossRef152
V. Tepavcevic, W. F. Blakemore. (2005) Glial grafting for demyelinating disease. Philosophical Transactions of the Royal Society B: Biological Sciences 360:1461, 1775-1795
CrossRef153
Wolfgang Brück. (2005) Clinical implications of neuropathological findings in multiple sclerosis. Journal of Neurology 252:S3, iii10-iii14
CrossRef154
Sarah K. Williams, Heather J. Spence, Ryan R. Rodgers, Bradford W. Ozanne, Una FitzGerald, Susan C. Barnett. (2005) Role of Mayven, a kelch-related protein in oligodendrocyte process formation. Journal of Neuroscience Research 81:5, 622-631
CrossRef155
Stephen A Back, Therese M F Tuohy, Hanqin Chen, Nicholas Wallingford, Andrew Craig, Jaime Struve, Ning Ling Luo, Fatima Banine, Ying Liu, Ansi Chang, Bruce D Trapp, Bruce F Bebo,, Mahendra S Rao, Larry S Sherman. (2005) Hyaluronan accumulates in demyelinated lesions and inhibits oligodendrocyte progenitor maturation. Nature Medicine
CrossRef156
François Lachapelle, Corinne Bachelin, Pierre Moissonnier, Brahim Nait-Oumesmar, Antoine Hidalgo, Denys Fontaine, Anne Baron-Van Evercooren. (2005) Failure of Remyelination in the Nonhuman Primate Optic Nerve. Brain Pathology 15:3, 198-207
CrossRef157
Alberto Perez-Bouza, Tamara Glaser, Oliver Brüstle. (2005) ES Cell-Derived Glial Precursors Contribute to Remyelination in Acutely Demyelinated Spinal Cord Lesions. Brain Pathology 15:3, 208-216
CrossRef158
Hans Lassmann. (2005) Stem cell and progenitor cell transplantation in multiple sclerosis: The discrepancy between neurobiological attraction and clinical feasibility. Journal of the Neurological Sciences 233:1-2, 83-86
CrossRef159
Chao Zhao, Stephen P.J. Fancy, Mark R. Kotter, Wen-Wu Li, Robin J.M. Franklin. (2005) Mechanisms of CNS remyelination—the key to therapeutic advances. Journal of the Neurological Sciences 233:1-2, 87-91
CrossRef160
Joshua C. Murtie, Yong-Xing Zhou, Tuan Q. Le, Adam C. Vana, Regina C. Armstrong. (2005) PDGF and FGF2 pathways regulate distinct oligodendrocyte lineage responses in experimental demyelination with spontaneous remyelination. Neurobiology of Disease 19:1-2, 171-182
CrossRef161
Catherine Lubetzki, Anna Williams, Bruno Stankoff. (2005) Promoting repair in multiple sclerosis: problems and prospects. Current Opinion in Neurology 18:3, 237-244
CrossRef162
Nobuo Terada, Grahame J. Kidd, Mike Kinter, Carl Bjartmar, Kim Moran-Jones, Bruce D. Trapp. (2005) ?IV tubulin is selectively expressed by oligodendrocytes in the central nervous system. Glia 50:3, 212-222
CrossRef163
T. Magnus, M. S. Rao. (2005) Neural stem cells in inflammatory CNS diseases: mechanisms and therapy. Journal of Cellular and Molecular Medicine 9:2, 303-319
CrossRef164
Laura Calzà, Mercedes Fernandez, Alessandro Giuliani, Giulia D'Intino, Stefania Pirondi, Sandra Sivilia, Michela Paradisi, Nadia DeSordi, Luciana Giardino. (2005) Thyroid hormone and remyelination in adult central nervous system: a lesson from an inflammatory-demyelinating disease. Brain Research Reviews 48:2, 339-346
CrossRef165
Arthur M. Butt, Jennifer Dinsdale. (2005) Fibroblast growth factor 2 induces loss of adult oligodendrocytes and myelin in vivo. Experimental Neurology 192:1, 125-133
CrossRef166
Catherine Fressinaud. (2005) Repeated injuries dramatically affect cells of the oligodendrocyte lineage: Effects of PDGF and NT-3 in vitro. Glia 49:4, 555-566
CrossRef167
Claudia F. Lucchinetti, Joseph Parisi, Wolfgang Bruck. (2005) The pathology of multiple sclerosis. Neurologic Clinics 23:1, 77-105
CrossRef168
Olaf Maier, Tiemen van der Heide, Anne-Marie van Dam, Wia Baron, Hans de Vries, Dick Hoekstra. (2005) Alteration of the extracellular matrix interferes with raft association of neurofascin in oligodendrocytes. Potential significance for multiple sclerosis?. Molecular and Cellular Neuroscience 28:2, 390-401
CrossRef169
Kristy Boyle, Michael F. Azari, Christos Profyris, Steven Petratos. (2005) Molecular mechanisms in schwann cell survival and death during peripheral nerve development, injury and disease. Neurotoxicity Research 7:1-2, 151-167
CrossRef170
Francesca Ruffini, Nathalie Arbour, Manon Blain, André Olivier, Jack P. Antel. (2004) Distinctive Properties of Human Adult Brain-Derived Myelin Progenitor Cells. The American Journal of Pathology 165:6, 2167-2175
CrossRef171
Eric Birgbauer, Tadimeti S. Rao, Michael Webb. (2004) Lysolecithin induces demyelination in vitro in a cerebellar slice culture system. Journal of Neuroscience Research 78:2, 157-166
CrossRef172
Steven Petratos, Michael F. Gonzales, Michael F. Azari, Mark Marriott, Rebecca A. Minichiello, Kylie A Shipham, Christos Profyris, Antonis Nicolaou, Kristy Boyle, Surindar S. Cheema, Trevor J. Kilpatrick. (2004) Expression of the low-affinity neurotrophin receptor, p75NTR, is upregulated by oligodendroglial progenitors adjacent to the subventricular zone in response to demyelination. Glia 48:1, 64-75
CrossRef173
Stefano Pluchino, Roberto Furlan, Gianvito Martino. (2004) Cell-based remyelinating therapies in multiple sclerosis: evidence from experimental studies. Current Opinion in Neurology 17:3, 247-255
CrossRef174
Francesca Ruffini, Timothy E. Kennedy, Jack P. Antel. (2004) Inflammation and Remyelination in the Central Nervous System. The American Journal of Pathology 164:5, 1519-1522
CrossRef175
Jeffrey L. Mason, Arrel Toews, Janell D. Hostettler, Pierre Morell, Kinuko Suzuki, James E. Goldman, Glenn K. Matsushima. (2004) Oligodendrocytes and Progenitors Become Progressively Depleted within Chronically Demyelinated Lesions. The American Journal of Pathology 164:5, 1673-1682
CrossRef176
Martin Stangel. (2004) Remyelinating and neuroprotective treatments in multiple sclerosis. Expert Opinion on Investigational Drugs 13:4, 331-347
CrossRef177
Rachel H Woodruff, Marcus Fruttiger, William D Richardson, Robin J.M Franklin. (2004) Platelet-derived growth factor regulates oligodendrocyte progenitor numbers in adult CNS and their response following CNS demyelination. Molecular and Cellular Neuroscience 25:2, 252-262
CrossRef178
Anna Setzu, Charles Ffrench-Constant, Robin J.M. Franklin. (2004) CNS axons retain their competence for myelination throughout life. Glia 45:3, 307-311
CrossRef179
Laurent Magy, Caroline Mertens, Virginia Avellana-Adalid, Mahamane Keita, François Lachapelle, Brahim Nait-Oumesmar, Bertrand Fontaine, Anne Baron-Van Evercooren. (2003) Inducible expression of FGF2 by a rat oligodendrocyte precursor cell line promotes CNS myelination in vitro. Experimental Neurology 184:2, 912-922
CrossRef180
R. Letourneau, J.J. Rozniecki, V. Dimitriadou, T.C. Theoharides. (2003) Ultrastructural evidence of brain mast cell activation without degranulation in monkey experimental allergic encephalomyelitis. Journal of Neuroimmunology 145:1-2, 18-26
CrossRef181
Christopher B. Lock, Renu A. Heller. (2003) Gene microarray analysis of multiple sclerosis lesions. Trends in Molecular Medicine 9:12, 535-541
CrossRef182
Bogoljub Ciric, Charles L. Howe, Mateo Paz Soldan, Arthur E. Warrington, Allan J. Bieber, Virginia Keulen, Moses Rodriguez, Larry R. Pease. (2003) Human Monoclonal IgM Antibody Promotes CNS Myelin Repair Independent of Fc Function. Brain Pathology 13:4, 608-616
CrossRef183
D.M. Chari, W.L. Huang, W.F. Blakemore. (2003) Dysfunctional oligodendrocyte progenitor cell (OPC) populations may inhibit repopulation of OPC depleted tissue. Journal of Neuroscience Research 73:6, 787-793
CrossRef184
Isabelle Jean, Catherine Fressinaud. (2003) Spontaneous central nervous system remyelination is not altered in NFH-lacZ transgenic mice after chemical demyelination. Journal of Neuroscience Research 73:1, 54-60
CrossRef185
Mark F. Stidworthy, Stephane Genoud, Ueli Suter, Ned Mantei, Robin J. M. Franklin. (2003) Quantifying the Early Stages of Remyelination Following Cuprizone-induced Demyelination. Brain Pathology 13:3, 329-339
CrossRef186
Bernd C. Kieseier, Hans-Peter Hartung. (2003) Multiple paradigm shifts in multiple sclerosis. Current Opinion in Neurology 16:3, 247-252
CrossRef187
Hans A. Boer. (2003) The Work of Andrew Weil and Deepak Chopra-Two Holistic Health/New Age Gurus: A Critique of the Holistic Health/New Age Movements. Medical Anthropology Quarterly 17:2, 233-250
CrossRef188
Trevor Owens. (2003) The enigma of multiple sclerosis: inflammation and neurodegeneration cause heterogeneous dysfunction and damage. Current Opinion in Neurology 16:3, 259-265
CrossRef189
Harald Neumann. (2003) Molecular mechanisms of axonal damage in inflammatory central nervous system diseases. Current Opinion in Neurology 16:3, 267-273
CrossRef190
Scott S Zamvil, Lawrence Steinman. (2003) Diverse Targets for Intervention during Inflammatory and Neurodegenerative Phases of Multiple Sclerosis. Neuron 38:5, 685-688
CrossRef191
Emmanuelle Waubant. (2003) Emerging disease modifying therapies for multiple sclerosis. Expert Opinion on Emerging Drugs 8:1, 145-161
CrossRef192
Heinz Wiendl, Bernd C Kieseier. (2003) Disease-modifying therapies in multiple sclerosis: an update on recent and ongoing trials and future strategies. Expert Opinion on Investigational Drugs 12:4, 689-712
CrossRef193
Patrizia Casaccia-Bonnefil, Aixiao Liu. (2003) Relationship between cell cycle molecules and onset of oligodendrocyte differentiation. Journal of Neuroscience Research 72:1, 1-11
CrossRef194
Oliver Neuhaus, Juan J. Archelos, Hans-Peter Hartung. (2003) Immunomodulation in multiple sclerosis: from immunosuppression to neuroprotection. Trends in Pharmacological Sciences 24:3, 131-138
CrossRef195
Martin Kerschensteiner, Christine Stadelmann, Georg Dechant, Hartmut Wekerle, Reinhard Hohlfeld. (2003) Neurotrophic cross-talk between the nervous and immune systems: Implications for neurological diseases. Annals of Neurology 53:3, 292-304
CrossRef196
Wolfgang Brück, Tanja Kuhlmann, Christine Stadelmann. (2003) Remyelination in multiple sclerosis. Journal of the Neurological Sciences 206:2, 181-185
CrossRef197
K Ohta. (2003) Dissociative increase of oligodendrocyte progenitor cells between young and aged rats after transient cerebral ischemia. Neuroscience Letters 335:3, 159-162
CrossRef198
Peter M Mathisen. (2003) Gene discovery and validation for neurodegenerative diseases. Drug Discovery Today 8:1, 39-46
CrossRef199
Martin Stangel, Hans-Peter Hartung. (2002) Remyelinating strategies for the treatment of multiple sclerosis. Progress in Neurobiology 68:5, 361-376
CrossRef200
Melissa A. Cosenza, Meng-Liang Zhao, Sai L. Shankar, Bridget Shafit-Zagardo, Sunhee C. Lee. (2002) Up-regulation of MAP2e-expressing oligodendrocytes in the white matter of patients with HIV-1 encephalitis. Neuropathology and Applied Neurobiology 28:6, 480-488
CrossRef201
David H. Rowitch, Q.Richard Lu, Nicoletta Kessaris, William D. Richardson. (2002) An ‘oligarchy’ rules neural development. Trends in Neurosciences 25:8, 417-422
CrossRef202
Jeff W. M. Bulte, Ian D. Duncan, Joseph A. Frank. (2002) In Vivo Magnetic Resonance Tracking of Magnetically Labeled Cells After Transplantation. Journal of Cerebral Blood Flow & Metabolism899-907
CrossRef203
Ihab R. Dorotta, Armin Schubert. (2002) Multiple sclerosis and anesthetic implications. Current Opinion in Anaesthesiology 15:3, 365-370
CrossRef204
Christian Confavreux, Sandra Vukusic. (2002) Natural history of multiple sclerosis: implications for counselling and therapy. Current Opinion in Neurology 15:3, 257-266
CrossRef205
Paty, Donald W., , Arnold, Douglas L., . (2002) The Lesions of Multiple Sclerosis. New England Journal of Medicine 346:3, 199-200
Full Text
