Publications
187 results found
Anderson JM, Patani R, Reynolds R, et al., 2009, Evidence for abnormal tau phosphorylation in early aggressive multiple sclerosis, ACTA NEUROPATHOLOGICA, Vol: 117, Pages: 583-589, ISSN: 0001-6322
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- Citations: 33
Papadopoulos D, Dukes S, Patel R, et al., 2009, Substantial Archaeocortical Atrophy and Neuronal Loss in Multiple Sclerosis, BRAIN PATHOLOGY, Vol: 19, Pages: 238-253, ISSN: 1015-6305
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- Citations: 152
Serafini B, Magliozzi R, Rosicarelli B, et al., 2008, Expression of TWEAK and Its Receptor Fn14 in the Multiple Sclerosis Brain: Implications for Inflammatory Tissue Injury, JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, Vol: 67, Pages: 1137-1148, ISSN: 0022-3069
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- Citations: 40
Anderson JM, Hampton DW, Patani R, et al., 2008, Abnormally phosphorylated tau is associated with neuronal and axonal loss in experimental autoimmune encephalomyelitis and multiple sclerosis, BRAIN, Vol: 131, Pages: 1736-1748, ISSN: 0006-8950
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- Citations: 101
Sargiannidou I, Ahn M, Enriquez AD, et al., 2008, Human oligodendrocytes express Cx31.3: Function and interactions with Cx32 mutants, NEUROBIOLOGY OF DISEASE, Vol: 30, Pages: 221-233, ISSN: 0969-9961
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- Citations: 35
Zeis T, Graumann U, Reynolds R, et al., 2008, Normal-appearing white matter in multiple sclerosis is in a subtle balance between inflammation and neuroprotection, BRAIN, Vol: 131, Pages: 288-303, ISSN: 0006-8950
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- Citations: 156
Scheiermann C, Meda P, Aurrand-Lions M, et al., 2007, Expression and function of junctional adhesion molecule-C in myelinated peripheral nerves, SCIENCE, Vol: 318, Pages: 1472-1475, ISSN: 0036-8075
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- Citations: 49
Serafini B, Rosicarelli B, Franciotta D, et al., 2007, Dysregulated Epstein-Barr virus infection in the multiple sclerosis brain, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 204, Pages: 2899-2912, ISSN: 0022-1007
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- Citations: 528
Patani R, Balaratnam M, Vora A, et al., 2007, Remyelination can be extensive in multiple sclerosis despite a long disease course, NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, Vol: 33, Pages: 277-287, ISSN: 0305-1846
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- Citations: 226
Schmitt A, Bauer M, Heinsen H, et al., 2007, How a neuropsychiatric brain bank should be run: a consensus paper of Brainnet Europe II, JOURNAL OF NEURAL TRANSMISSION, Vol: 114, Pages: 527-537, ISSN: 0300-9564
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- Citations: 40
Magliozzi R, Howell O, Vora A, et al., 2007, Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology, BRAIN, Vol: 130, Pages: 1089-1104, ISSN: 0006-8950
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- Citations: 985
Nait-Oumesmar B, Picard-Riera N, Kerninon C, et al., 2007, Activation of the subventricular zone in multiple sclerosis: Evidence for early glial progenitors, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 104, Pages: 4694-4699, ISSN: 0027-8424
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- Citations: 257
Coman I, Aigrot MS, Seilhean D, et al., 2006, Nodal, paranodal and juxtaparanodal axonal proteins during demyelination and remyelination in multiple sclerosis, BRAIN, Vol: 129, Pages: 3186-3195, ISSN: 0006-8950
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- Citations: 159
Howell OW, Palser A, Polito A, et al., 2006, Disruption of neurofascin localization reveals early changes preceding demyelination and remyelination in multiple sclerosis, BRAIN, Vol: 129, Pages: 3173-3185, ISSN: 0006-8950
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- Citations: 145
Papadopoulos D, Ewans L, Pham-Dinh D, et al., 2006, Upregulation of α-synuclein in neurons and glia in inflammatory demyelinating disease, MOLECULAR AND CELLULAR NEUROSCIENCE, Vol: 31, Pages: 597-612, ISSN: 1044-7431
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- Citations: 38
Papadopoulos D, Pham-Dinh D, Reynolds R, 2006, Axon loss is responsible for chronic neurological deficit following inflammatory demyelination in the rat, EXPERIMENTAL NEUROLOGY, Vol: 197, Pages: 373-385, ISSN: 0014-4886
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- Citations: 90
Polito A, Reynolds R, 2005, NG2-expressing cells as oligodendrocyte progenitors in the normal and demyelinated adult central nervous system, JOURNAL OF ANATOMY, Vol: 207, Pages: 707-716, ISSN: 0021-8782
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- Citations: 186
Anderson AA, Kendal CE, Garcia-Maya M, et al., 2005, A peptide from the first fibronectin domain of NCAM acts as an inverse agonist and stimulates FGF receptor activation, neurite outgrowth and survival, JOURNAL OF NEUROCHEMISTRY, Vol: 95, Pages: 570-583, ISSN: 0022-3042
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- Citations: 48
Cynthia Benz, Richard Reynolds, 2005, Coping with Multiple Sclerosis, London, Publisher: Vermilion, ISBN: 9780091902469
Miller R, Reynolds R, 2004, Oligodendroglial Lineage, Myelin Biology and Disorders, Pages: 289-310, ISBN: 9780124395107
The oligodendrocyte lineage is derived from cells of the neural tube. Presumably, early in development, all neural tube cells have the capacity to generate oligodendrocytes, although during the course of normal embryogenesis, only some cells manifest that potential. Oligodendrocyte precursors undergo a number of structural and biochemical changes as they mature. Structurally, the cells begin to develop a more complex morphology and frequently develop multiple processes, although they retain a relatively large cell body. Biochemically, maturing oligodendrocyte precursors begin to express antigens on their surface that bind the monoclonal antibody O4. In conclusion, the adult CNS contains a substantial population of slowly dividing cells with the phenotype of oligodendroglial progenitors. Their number and location in the resting CNS is suggestive of a number of additional roles that are yet to be explored. © 2004 Elsevier Inc. All rights reserved.
Graumann U, Reynolds R, Steck AJ, et al., 2003, Molecular changes in normal appearing white matter in multiple sclerosis are characteristic of neuroprotective mechanisms against hypoxic insult, BRAIN PATHOLOGY, Vol: 13, Pages: 554-573, ISSN: 1015-6305
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- Citations: 176
Dawson MRL, Polito A, Levine JM, et al., 2003, NG2-expressing glial progenitor cells: an abundant and widespread population of cycling cells in the adult rat CNS, MOLECULAR AND CELLULAR NEUROSCIENCE, Vol: 24, Pages: 476-488, ISSN: 1044-7431
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- Citations: 660
Charles P, Reynolds R, Seilhean D, et al., 2002, Re-expression of PSA-NCAM by demyelinated axons: an inhibitor of remyelination in multiple sclerosis?, BRAIN, Vol: 125, Pages: 1972-1979, ISSN: 0006-8950
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- Citations: 218
Reynolds R, Dawson M, Papadopoulos D, et al., 2002, The response of NG2-expressing oligodendrocyte progenitors to demyelination in MOG-EAE and MS, JOURNAL OF NEUROCYTOLOGY, Vol: 31, Pages: 523-536, ISSN: 0300-4864
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- Citations: 140
Charles P, Reynolds R, Seilhean D, et al., 2002, Re-expression of PSA-NCAM by demyelinated axons: An inhibitor of remyelination in multiple sclerosis?, Brain, Vol: 125, Pages: 1972-1979, ISSN: 0006-8950
Multiple sclerosis is affecting ∼1 out of every 1000 individuals in the western world. After axons are denuded of myelin in the early stages of the disease, remyelination occurs, but eventually this process fails, and permanent disability is the result. During development, the polysialylated form of the neural cell adhesion molecule NCAM, PSA-NCAM, is expressed at the axonal surface and acts as a negative regulator of myelination, presumably by preventing myelin-forming cells from attaching to the axon. Removal of PSA-NCAM from the axonal surface is a prerequisite for the initiation of myelination. We questioned whether, in multiple sclerosis, reexpression of PSA-NCAM by axons could occur, and therefore account for the failure of remyelination. Forty multiple sclerosis lesions from 24 different post-mortem multiple sclerosis cases were selected by histological methods and analysed by immunohistochemistry. Demyelinated lesions and partially remyelinated lesions (shadow plaques) were studied. Controls consisted of post-mortem brain tissue from patients with amyotrophic lateral sclerosis and without neurological disease. We showed that PSA-NCAM, normally absent from adult brain, is re-expressed on demyelinated axons in the plaques. Within shadow plaques, remyelinated axons do not express PSA-NCAM. Re-expression of PSA-NCAM could act as an inhibitor of remyelination and participate in disease progression in multiple sclerosis.
Orian JM, Ahern AJ, Ayers MM, et al., 2001, Disturbed oligodendrocyte development and recovery from hypomyelination in a c-myc transgenic mouse mutant, JOURNAL OF NEUROSCIENCE RESEARCH, Vol: 66, Pages: 46-58, ISSN: 0360-4012
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- Citations: 5
Wu HY, Dawson MRL, Reynolds R, et al., 2001, Expression of QKI proteins and MAP1B identifies actively myelinating oligodendrocytes in adult rat brain, MOLECULAR AND CELLULAR NEUROSCIENCE, Vol: 17, Pages: 292-302, ISSN: 1044-7431
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- Citations: 50
Levine JM, Reynolds R, Fawcett JW, 2001, The oligodendrocyte precursor cell in health and disease, TRENDS IN NEUROSCIENCES, Vol: 24, Pages: 39-47, ISSN: 0166-2236
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- Citations: 556
Reynolds R, Cenci di Bello I, Dawson M, et al., 2001, The response of adult oligodendrocyte progenitors to demyelination in EAE., Prog Brain Res, Vol: 132, Pages: 165-174, ISSN: 0079-6123
Cells with the phenotypic characteristics of oligodendrocyte progenitors (NG2+/PDGF alpha R+/O4+) are found throughout the adult mammalian CNS in numbers similar to microglia. They are a reactive glial cell population and respond to demyelination by increasing in number, thereby repopulating the lesion site with cells capable of differentiating into remyelinating oligodendrocytes. Direct evidence that they differentiate into remyelinating cells is missing, although this is the most likely scenario. Cells with the same phenotype are found in normal human CNS tissue and also in chronic MS lesions. Further studies on this intriguing cell type are necessary in order to understand the molecular signals involved in their reaction to injury, particularly in multiple sclerosis.
Dawson MRL, Levine JM, Reynolds R, 2000, NG2-Expressing cells in the central nervous system: Are they oligodendroglial progenitors?, JOURNAL OF NEUROSCIENCE RESEARCH, Vol: 61, Pages: 471-479, ISSN: 0360-4012
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- Citations: 325
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