A Compston

Summary

Affiliation: University of Cambridge
Country: UK

Publications

  1. ncbi request reprint Oligodendroglia are protected from antibody-mediated complement injury by normal immunoglobulins ("IVIg")
    M Stangel
    Neurology Unit, Addenbrooke s Hospital, University of Cambridge, UK
    J Neuroimmunol 103:195-201. 2000
  2. ncbi request reprint A genome-wide screen for linkage disequilibrium in Australian HLA-DRB1*1501 positive multiple sclerosis patients
    M Ban
    Neurology Unit, Addenbrooke s Hospital, University of Cambridge, Cambridge CB2 2QQ, UK
    J Neuroimmunol 143:60-4. 2003
  3. ncbi request reprint A genome wide linkage disequilibrium screen in Parkinson's disease
    Thomas Foltynie
    Dept of Neurology, University of Cambridge, Cambridge, CB2 2PY, UK
    J Neurol 252:597-602. 2005
  4. ncbi request reprint Recurrent myelitis and optic neuritis in a 29-year-old woman
    Amanda Cox
    Department of Clinical Neurosciences, University of Cambridge, UK
    Lancet Neurol 4:510-6. 2005
  5. ncbi request reprint A genome-wide DNA microsatellite association screen to identify chromosomal regions harboring candidate genes in diabetic nephropathy
    Amy Jayne McKnight
    Nephrology Research Group, Department of Epidemiology and Public Health, Queen s University Belfast, Northern Ireland
    J Am Soc Nephrol 17:831-6. 2006
  6. pmc The mesenchymal stem cells in multiple sclerosis (MSCIMS) trial protocol and baseline cohort characteristics: an open-label pre-test: post-test study with blinded outcome assessments
    Peter Connick
    Dept, of Clinical Neurosciences, University of Cambridge, UK
    Trials 12:62. 2011
  7. ncbi request reprint The pathogenesis and basis for treatment in multiple sclerosis
    Alastair Compston
    School of Clinical Medicine, University of Cambridge Neurology, Addenbrooke s Hospital, Hills Road, Cambridge CB2 2QQ, UK
    Clin Neurol Neurosurg 106:246-8. 2004
  8. ncbi request reprint The basis for treatment in multiple sclerosis
    A Compston
    Department of Clinical Neurosciences, University of Cambridge Clinical School, Cambridge, UK
    Acta Neurol Scand Suppl 183:41-7. 2006
  9. ncbi request reprint Multiple sclerosis
    Alastair Compston
    Neurology Unit, University of Cambridge Clinical School, Addenbrooke s Hospital, Cambridge CB2 2QQ, UK
    Lancet 359:1221-31. 2002
  10. ncbi request reprint Genetic analysis of multiple sclerosis
    Alastair Compston
    University of Cambridge Neurology Unit, Addenbrooke s Hospital, Hills Road, Cambridge CB2 2QQ, United Kingdom
    Curr Neurol Neurosci Rep 2:259-66. 2002

Detail Information

Publications99

  1. ncbi request reprint Oligodendroglia are protected from antibody-mediated complement injury by normal immunoglobulins ("IVIg")
    M Stangel
    Neurology Unit, Addenbrooke s Hospital, University of Cambridge, UK
    J Neuroimmunol 103:195-201. 2000
    ..Inhibition of inflammatory mechanisms, as opposed to a direct effect on remyelinating cells, may underlie the role of IVIg in promoting myelin repair in experimental models...
  2. ncbi request reprint A genome-wide screen for linkage disequilibrium in Australian HLA-DRB1*1501 positive multiple sclerosis patients
    M Ban
    Neurology Unit, Addenbrooke s Hospital, University of Cambridge, Cambridge CB2 2QQ, UK
    J Neuroimmunol 143:60-4. 2003
    ..Further analysis of these regions is required to establish whether the associations observed are due to epistatic interaction with the HLA locus...
  3. ncbi request reprint A genome wide linkage disequilibrium screen in Parkinson's disease
    Thomas Foltynie
    Dept of Neurology, University of Cambridge, Cambridge, CB2 2PY, UK
    J Neurol 252:597-602. 2005
    ..Subgroup analysis of the most promising marker shows some evidence that microsatellite marker D1S2886 is associated with familial forms of the disease...
  4. ncbi request reprint Recurrent myelitis and optic neuritis in a 29-year-old woman
    Amanda Cox
    Department of Clinical Neurosciences, University of Cambridge, UK
    Lancet Neurol 4:510-6. 2005
  5. ncbi request reprint A genome-wide DNA microsatellite association screen to identify chromosomal regions harboring candidate genes in diabetic nephropathy
    Amy Jayne McKnight
    Nephrology Research Group, Department of Epidemiology and Public Health, Queen s University Belfast, Northern Ireland
    J Am Soc Nephrol 17:831-6. 2006
    ....
  6. pmc The mesenchymal stem cells in multiple sclerosis (MSCIMS) trial protocol and baseline cohort characteristics: an open-label pre-test: post-test study with blinded outcome assessments
    Peter Connick
    Dept, of Clinical Neurosciences, University of Cambridge, UK
    Trials 12:62. 2011
    ..Illustrated by the MSCIMS trial protocol, we describe a novel methodology based on detailed assessment of the anterior visual pathway as a model of wider disease processes--the "sentinel lesion approach"...
  7. ncbi request reprint The pathogenesis and basis for treatment in multiple sclerosis
    Alastair Compston
    School of Clinical Medicine, University of Cambridge Neurology, Addenbrooke s Hospital, Hills Road, Cambridge CB2 2QQ, UK
    Clin Neurol Neurosurg 106:246-8. 2004
    ....
  8. ncbi request reprint The basis for treatment in multiple sclerosis
    A Compston
    Department of Clinical Neurosciences, University of Cambridge Clinical School, Cambridge, UK
    Acta Neurol Scand Suppl 183:41-7. 2006
    ....
  9. ncbi request reprint Multiple sclerosis
    Alastair Compston
    Neurology Unit, University of Cambridge Clinical School, Addenbrooke s Hospital, Cambridge CB2 2QQ, UK
    Lancet 359:1221-31. 2002
    ..Despite limited success in each of these categories, everyone touched by multiple sclerosis looks for a better dividend from applying an improved understanding of the pathogenesis to clinical management...
  10. ncbi request reprint Genetic analysis of multiple sclerosis
    Alastair Compston
    University of Cambridge Neurology Unit, Addenbrooke s Hospital, Hills Road, Cambridge CB2 2QQ, United Kingdom
    Curr Neurol Neurosci Rep 2:259-66. 2002
    ..When eventually in place, the potential of this genetic knowledge for improved understanding of the pathogenesis of multiple sclerosis and designing novel treatments is considerable...
  11. pmc The genetic epidemiology of multiple sclerosis
    A Compston
    University of Cambridge Neurology Unit, Addenbrooke s Hospital, UK
    Philos Trans R Soc Lond B Biol Sci 354:1623-34. 1999
    ..Genotypic and phenotypic analyses are beginning to question this assumption. A major part of future studies in the genetics of MS will be to resolve the question of disease heterogeneity...
  12. ncbi request reprint Complexity and heterogeneity in demyelinating disease
    Alastair Compston
    Department of Clinical Neurosciences, University of Cambridge Clinical School, Cambridge, CB1 2QQ, UK
    Brain 130:1178-80. 2007
  13. pmc Efficient derivation of NPCs, spinal motor neurons and midbrain dopaminergic neurons from hESCs at 3% oxygen
    S R L Stacpoole
    Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
    Nat Protoc 6:1229-40. 2011
    ..The ability to generate defined cell types at 3% O(2) should represent a significant advancement for in vitro disease modeling and potentially for cell-based therapies...
  14. ncbi request reprint A role for oligodendrocyte-derived IGF-1 in trophic support of cortical neurons
    A Wilkins
    Cambridge Centre for Brain Repair, Cambridge, UK
    Glia 36:48-57. 2001
    ..This study provides evidence that OPCs and differentiated oligodendrocytes support neuronal survival by both contact-mediated and soluble mechanisms and that IGF-1 significantly contributes to this effect...
  15. ncbi request reprint A genome screen for multiple sclerosis in Italian families
    S Broadley
    University of Cambridge Neurology Unit, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 2QQ, UK
    Genes Immun 2:205-10. 2001
    ..Overall these results have refined the linkage data relating to this disease in Italians modestly supporting some previously identified areas of interest and helping to exclude others...
  16. ncbi request reprint Refining the analysis of a whole genome linkage disequilibrium association map: the United Kingdom results
    Tai Wai Yeo
    University of Cambridge Neurology Unit, Addenbrook s Hospital, Hills Road, Cambridge CB2 2QQ, UK
    J Neuroimmunol 143:53-9. 2003
    ....
  17. ncbi request reprint A genome-wide screen for linkage disequilibrium in Sardinian multiple sclerosis
    Francesca Coraddu
    Neurology Unit, Addenbrooks Hospital, University of Cambridge, Hills Road, Cambridge CB2 2QQ, UK
    J Neuroimmunol 143:120-3. 2003
    ..Five of these markers-D2S408 (2q36), D6S271 (6p21), D6S344 (6p25), D7S1818 (7p12) and D16S420 (16p12)-remained nominally significant in both studies after conservative refining analysis...
  18. ncbi request reprint A whole genome screen for linkage disequilibrium in multiple sclerosis confirms disease associations with regions previously linked to susceptibility
    Stephen Sawcer
    University of Cambridge Neurology Unit, Addenbrooke s Hospital, Cambridge, UK
    Brain 125:1337-47. 2002
    ....
  19. ncbi request reprint Mechanisms of axon-glial injury of the optic nerve
    A Compston
    Department of Clinical Neurosciences, University of Cambridge, Clinical School, Addenbrooke s Hospital, Hills Road, Cambridge, UK
    Eye (Lond) 18:1182-7. 2004
    ..Hence, in the context of brain inflammation, there is an inseparable interplay between immunological and neurobiological contributions to tissue injury...
  20. ncbi request reprint Polyclonal immunoglobulins for intravenous use do not influence the behaviour of cultured oligodendrocytes
    M Stangel
    MRC Cambridge Centre for Brain Repair, Neurology Unit, Addenbrooke s Hospital, University of Cambridge, UK
    J Neuroimmunol 96:228-33. 1999
    ..These results argue against a direct effect of IVIg on remyelination and are in favour of an indirect yet not clearly defined mechanism that supports remyelination...
  21. ncbi request reprint Heterogeneity at the HLA-DRB1 locus and risk for multiple sclerosis
    Lisa F Barcellos
    Division of Epidemiology, School of Public Health, University of California, Berkeley 94720, USA, and Department of Clinical Neurosciences, University of Cambridge, Addenbrooke s Hospital, UK
    Hum Mol Genet 15:2813-24. 2006
    ....
  22. ncbi request reprint Environmental signals regulate lineage choice and temporal maturation of neural stem cells from human embryonic stem cells
    Alexis J Joannides
    Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
    Brain 130:1263-75. 2007
    ..Controlled manipulation of environmental signals appropriate to the pathological specificity of the targeted disease will be necessary in the design of therapeutic stem cell-based strategies...
  23. ncbi request reprint A genome screen for multiple sclerosis in Sardinian multiplex families
    F Coraddu
    University of Cambridge Neurology Unit, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 2QQ, UK
    Eur J Hum Genet 9:621-6. 2001
    ..We have performed a whole genome screen for linkage in 49 Sardinian multiplex families using 327 markers. Non parametric linkage analysis of these data reveal suggestive linkage in the region of Chr 1q31, Chr 10q23 and Chr 11p15...
  24. ncbi request reprint Inhibition of tumour necrosis factor-alpha (TNFalpha)-induced NF-kappaB p52 converts the metabolic effects of microglial-derived TNFalpha on mouse cerebellar neurones to neurotoxicity
    R S Nicholas
    University of Cambridge Neurology Unit, Addenbrooke's Hospital, Hills Road, Cambridge, UK
    J Neurochem 76:1431-8. 2001
    ..Characterizing and manipulating these events in vivo theoretically provides an opportunity for neuroprotection in selected diseases affecting the central nervous system...
  25. ncbi request reprint A novel role for Sema3A in neuroprotection from injury mediated by activated microglia
    Henry H Majed
    Department of Clinical Neurosciences, Centre for Brain Repair, University of Cambridge, Forvie Site, Cambridge CB2 2PY, United Kingdom
    J Neurosci 26:1730-8. 2006
    ..These results suggest a novel semaphorin-mediated mechanism of neuroprotection whereby stressed neurons can protect themselves from further damage by activated microglia...
  26. pmc Common variants near MC4R are associated with fat mass, weight and risk of obesity
    Ruth J F Loos
    MRC Epidemiology Unit, Addenbrooke s Hospital, Cambridge CB2 0QQ, UK
    Nat Genet 40:768-75. 2008
    ....
  27. pmc Multiple sclerosis in sibling pairs: an analysis of 250 families
    J Chataway
    University of Cambridge Neurology Unit, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 2QQ, UK
    J Neurol Neurosurg Psychiatry 71:757-61. 2001
    ..These results are consistent with the hypothesis that genes influence both disease susceptibility and evolution in multiple sclerosis...
  28. ncbi request reprint The genetic analysis of multiple sclerosis
    S Sawcer
    University of Cambridge Neurology Unit, Addenbrooke s Hospital, UK
    Trends Genet 13:234-9. 1997
    ....
  29. pmc A non-synonymous SNP within membrane metalloendopeptidase-like 1 (MMEL1) is associated with multiple sclerosis
    M Ban
    Department of Clinical Neuroscience, University of Cambridge, Addenbrooke s Hospital, Cambridge, UK
    Genes Immun 11:660-4. 2010
    ..A combined analysis of the nsSNP screen and replication data provides evidence implicating a novel additional locus, rs3748816 in membrane metalloendopeptidase-like 1 (MMEL1; odds ratio=1.16, P=3.54 × 10⁻⁶) in MS susceptibility...
  30. ncbi request reprint Regional potential for oligodendrocyte generation in the rodent embryonic spinal cord following exposure to EGF and FGF-2
    S Chandran
    MRC Cambridge Centre for Brain Repair, University of Cambridge, United Kingdom
    Glia 24:382-9. 1998
    ..The observation that from E14, the dorsal cord already has latent oligodendrogenic potential provides an alternative mechanism for oligodendrocyte formation to ventro-dorsal migration of oligodendrocyte precursors...
  31. ncbi request reprint Neural stem cells as a potential source of oligodendrocytes for myelin repair
    Siddharthan Chandran
    Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
    J Neurol Sci 233:179-81. 2005
    ..Inter-species difference in the capacity of neural precursors to generate oligodendrocytes emphasises the need for greater study of human derived stem cell populations...
  32. ncbi request reprint Trophic factors attenuate nitric oxide mediated neuronal and axonal injury in vitro: roles and interactions of mitogen-activated protein kinase signalling pathways
    Alastair Wilkins
    Department of Clinical Neurosciences and Centre for Brain Repair, University of Cambridge, Forvie Site, Robinson Way, Cambridge CB2 2PY, UK
    J Neurochem 92:1487-96. 2005
    ..This study emphasizes that different mechanisms may underlie neuronal/axonal destructive processes, and suggests that trophic factors may modulate NO-mediated neurone/axon destruction via specific pathways...
  33. pmc Myelin repair: the role of stem and precursor cells in multiple sclerosis
    Siddharthan Chandran
    Cambridge Centre for Brain Repair, University of Cambridge, Robinson Way, Cambridge CB2 2PY, UK
    Philos Trans R Soc Lond B Biol Sci 363:171-83. 2008
    ..This review considers the basic and clinical biology of remyelination and the potential contribution of stem and precursor cells to enhance and supplement spontaneous remyelination...
  34. ncbi request reprint Minocycline attenuates nitric oxide-mediated neuronal and axonal destruction in vitro
    Alastair Wilkins
    Centre for Brain Repair and Dept of Clinical Neurosciences, University of Cambridge, Forvie Site, Robinson Way, Cambridge CB2 2PY, UK
    Neuron Glia Biol 1:297-305. 2004
    ..These results indicate that, in addition to anti-inflammatory properties, minocycline has direct protective effects on neurons and provides further evidence for its use in disorders of the CNS...
  35. ncbi request reprint Differential generation of oligodendrocytes from human and rodent embryonic spinal cord neural precursors
    Siddharthan Chandran
    Department of Clinical Neurosciences, University of Cambridge, United Kingdom
    Glia 47:314-24. 2004
    ..These results provide further evidence for inter-species difference in the capacity of neural precursors to generate oligodendrocytes...
  36. ncbi request reprint Efficient generation of neural precursors from adult human skin: astrocytes promote neurogenesis from skin-derived stem cells
    Alexis Joannides
    Department of Clinical Neurosciences, University of Cambridge and Addenbrooke s Hospital, Cambridge, UK
    Lancet 364:172-8. 2004
    ..An alternative source of human neural stem cells is needed; a source that is readily accessible, easily expanded, and reliably induced to a neural fate...
  37. pmc A high-density screen for linkage in multiple sclerosis
    Stephen Sawcer
    University of Cambridge, Department of Clinical Neuroscience, Addenbrooke s Hospital, Hills Road, Cambridge, CB2 2QQ, United Kingdom
    Am J Hum Genet 77:454-67. 2005
    ....
  38. ncbi request reprint Minimally manipulated oligodendrocyte precursor cells retain exclusive commitment to the oligodendrocyte lineage following transplantation into intact and injured hippocampus
    Daniel J Webber
    Department of Clinical Neurosciences and Centre for Brain Repair, University of Cambridge, Forvie Site, Robinson Way, Cambridge, CB2 2PY, UK
    Eur J Neurosci 26:1791-800. 2007
    ..These findings show that unselected and unmanipulated populations of cortical OPCs remain as precursor cells, commit to the oligodendrocyte lineage and fail to respond to the extrinsic cues of a neurogenic or injured environment...
  39. ncbi request reprint Association of the truncating splice site mutation in BTNL2 with multiple sclerosis is secondary to HLA-DRB1*15
    James A Traherne
    Cambridge Institute for Medical Research, Wellcome Trust MRC Building, Cambridge, UK
    Hum Mol Genet 15:155-61. 2006
    ..The association of BTNL2 with MS observed in the African-American data set was also secondary to the primary DRB1*15 association...
  40. ncbi request reprint No evidence of a significant role for CTLA-4 in multiple sclerosis
    Richard H Roxburgh
    Department of Clinical Neurosciences, Cambridge University, Addenbrooke s Hospital, CB2 2QQ Cambridge, UK
    J Neuroimmunol 171:193-7. 2006
    ..No individual marker or common haplotype showed evidence of association with disease. These data suggest that any effect of CTLA-4 on multiple sclerosis susceptibility is likely to be very small...
  41. ncbi request reprint CD24 Ala/Val polymorphism and multiple sclerosis
    An Goris
    Department of Clinical Neurosciences, Neurology Unit, University of Cambridge, Addenbrooke s Hospital, Cambridge CB2 2QQ, UK
    J Neuroimmunol 175:200-2. 2006
    ..Since the CD24 gene is part of a segmental duplication, special care is required for the identification and genotyping of single nucleotide polymorphisms...
  42. ncbi request reprint A highly enriched niche of precursor cells with neuronal and glial potential within the hair follicle dermal papilla of adult skin
    David P J Hunt
    Cambridge Centre for Brain Repair, Cambridge, United Kingdom
    Stem Cells 26:163-72. 2008
    ..This strategy of targeting a highly enriched niche of sphere-forming cells provides a novel and efficient method for generating neuronal and glial cells from an accessible adult somatic source that is both defined and minimally invasive...
  43. ncbi request reprint Linkage disequilibrium screening for multiple sclerosis implicates JAG1 and POU2AF1 as susceptibility genes in Europeans
    Maria Ban
    University of Cambridge, Department of Clinical Neurosciences, Addenbrooke s Hospital, Hills Road, Cambridge, UK
    J Neuroimmunol 179:108-16. 2006
    ..Association mapping across the candidate genes implicated by these markers in 937 UK trio families revealed modestly associated haplotypes in JAG1 (p=0.019) on chromosome 20p12.2 and POU2AF1 (p=0.003) on chromosome 11q23.1...
  44. pmc A second major histocompatibility complex susceptibility locus for multiple sclerosis
    Tai Wai Yeo
    Department of Clinical Neurosciences, University of Cambridge, Addenbrooke s Hospital, Cambridge, United Kingdom
    Ann Neurol 61:228-36. 2007
    ..The possibility that other genes in the MHC independently influence susceptibility to multiple sclerosis has been suggested but remains unconfirmed...
  45. ncbi request reprint Campath-1H treatment of multiple sclerosis: lessons from the bedside for the bench
    Alasdair Coles
    Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 2QQ, UK
    Clin Neurol Neurosurg 106:270-4. 2004
  46. ncbi request reprint Different pathways for iNOS-mediated toxicity in vitro dependent on neuronal maturation and NMDA receptor expression
    Sabine Golde
    Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK
    J Neurochem 82:269-82. 2002
    ..Our results therefore extend existing evidence for NO-mediated toxicity and show a complex interaction between inflammatory and excitotoxic mechanisms of injury in mature neurones...
  47. ncbi request reprint Oligodendrocytes promote neuronal survival and axonal length by distinct intracellular mechanisms: a novel role for oligodendrocyte-derived glial cell line-derived neurotrophic factor
    Alastair Wilkins
    Cambridge Center for Brain Repair, Forvie Site, Cambridge CB2 2PY, United Kingdom
    J Neurosci 23:4967-74. 2003
    ..Therefore, we have shown that factors released by OPCs and oligodendrocytes induce the activation of distinct intracellular pathways within neurons, which have different functional effects on the cell...
  48. ncbi request reprint Refining the linkage analysis on chromosome 10 in 449 sib-pairs with multiple sclerosis
    Eva Akesson
    Neurology Unit, Addenbrooke s Hospital, University of Cambridge, Cambridge, UK
    J Neuroimmunol 143:31-8. 2003
    ..This additional genotyping increased the information extraction in the region from 52% to 79% and revealed increased support for linkage (MLS 2.5) peaking at 10p15...
  49. ncbi request reprint Enhancing linkage analysis of complex disorders: an evaluation of high-density genotyping
    Stephen J Sawcer
    University of Cambridge Neurology Unit, Addenbrooke s Hospital, UK
    Hum Mol Genet 13:1943-9. 2004
    ..The extent of additional information extracted is considerable, indicating that reanalysis of existing multiplex families using these newer systems would substantially increase power...
  50. doi request reprint Genome-wide association studies in multiple sclerosis: lessons and future prospects
    Anu Kemppinen
    Neurology Unit, Department of Clinical Neurosciences, University of Cambridge, UK
    Brief Funct Genomics 10:61-70. 2011
    ..Finally, many genetic risk variants for MS remain to be identified. In order to expose some of the loci with more modest effects, a GWAS in nearly 10,000 MS patients has recently been completed...
  51. doi request reprint Abnormal tau phosphorylation in primary progressive multiple sclerosis
    Jane Marian Anderson
    Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Forvie Site, Robinson Way, Cambridge, UK
    Acta Neuropathol 119:591-600. 2010
    ..These findings establish a platform for further study of the role of insoluble tau formation, including determining the relevance of glial tau pathology, in the neurodegenerative phase of MS...
  52. pmc Origins of gliogenic stem cell populations within adult skin and bone marrow
    David P Hunt
    Anne Maclaren Laboratory for Regenerative Medicine, MRC Centre for Stem Cell Biology and Regenerative Medicine, Forvie Site, University of Cambridge, Cambridge, United Kingdom
    Stem Cells Dev 19:1055-65. 2010
    ..We conclude that SKPs, rather than bone marrow-derived MSCs, represent a more defined and developmentally rational source for the study and generation of Schwann cells from readily accessible adult tissues...
  53. pmc IL-21 drives secondary autoimmunity in patients with multiple sclerosis, following therapeutic lymphocyte depletion with alemtuzumab (Campath-1H)
    Joanne L Jones
    Department of Clinical Neuroscience, University of Cambridge, Addenbrooke s Hospital, Cambridge, United Kingdom
    J Clin Invest 119:2052-61. 2009
    ..We propose that, by driving cycles of T cell expansion and apoptosis to excess, IL-21 increases the stochastic opportunities for T cells to encounter self antigen and, hence, for autoimmunity...
  54. pmc Replication analysis identifies TYK2 as a multiple sclerosis susceptibility factor
    Maria Ban
    Department of Clinical Neuroscience, Addenbrooke s, Hospital, University of Cambridge, Cambridge, UK
    Eur J Hum Genet 17:1309-13. 2009
    ....
  55. doi request reprint An experimental model of secondary progressive multiple sclerosis that shows regional variation in gliosis, remyelination, axonal and neuronal loss
    David W Hampton
    Cambridge Centre for Brain Repair, University of Cambridge, ED Adrian Building, Forvie Site, Robinson Way, Cambridge, CB2 2PY UK
    J Neuroimmunol 201:200-11. 2008
    ..Together with the clinical pattern, our findings identify chronic EAE as an excellent model of secondary progressive multiple sclerosis...
  56. ncbi request reprint FGF-dependent generation of oligodendrocytes by a hedgehog-independent pathway
    Siddharthan Chandran
    Cambridge Centre for Brain Repair, University of Cambridge, ED Adrian Building, Forvie Site, Robinson Way, Cambridge CB2 2PY, UK
    Development 130:6599-609. 2003
    ..These findings are compatible with the idea of a hedgehog independent pathway for oligodendrocyte generation from neural stem cells...
  57. pmc Induction of Olig2 precursors by FGF involves BMP signalling blockade at the Smad level
    Bilada Bilican
    Department of Clinical Neurosciences and Centre for Brain Repair, University of Cambridge, Cambridge, United Kingdom
    PLoS ONE 3:e2863. 2008
    ....
  58. pmc Investigation of the role of mitochondrial DNA in multiple sclerosis susceptibility
    Maria Ban
    Department of Clinical Neurosciences, University of Cambridge, Addenbrooke s Hospital, Cambridge, United Kingdom
    PLoS ONE 3:e2891. 2008
    ..These results add to the evidence suggesting that variation in mtDNA and nuclear encoded mitochondrial genes may contribute to disease susceptibility in multiple sclerosis...
  59. pmc Derivation of neural precursor cells from human ES cells at 3% O(2) is efficient, enhances survival and presents no barrier to regional specification and functional differentiation
    S R L Stacpoole
    University of Cambridge, Department of Clinical Neurosciences, Cambridge, UK
    Cell Death Differ 18:1016-23. 2011
    ..Together these findings support 3% O(2) as a physiologically relevant system to study stem cell-derived neuronal differentiation and function as well as to model neuronal injury...
  60. ncbi request reprint Tau and alpha-synuclein in susceptibility to, and dementia in, Parkinson's disease
    An Goris
    Department of Clinical Neurosciences Neurology Unit, University of Cambridge, Cambridge, United Kingdom
    Ann Neurol 62:145-53. 2007
    ..We investigated the genetic basis of susceptibility to and cognitive heterogeneity of this disease...
  61. ncbi request reprint The genetic analysis of multiple sclerosis in Europeans: concepts and design
    Stephen Sawcer
    Department of Clinical Neurosciences, Neurology Unit, Addenbrooke s Hospital, University of Cambridge, Hills Road, Cambridge CB2 2QQ, UK
    J Neuroimmunol 143:13-6. 2003
  62. pmc Activin/Nodal inhibition alone accelerates highly efficient neural conversion from human embryonic stem cells and imposes a caudal positional identity
    Rickie Patani
    Anne McLaren Laboratory for Regenerative Medicine and Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom
    PLoS ONE 4:e7327. 2009
    ..We therefore sought to investigate the independent influence of SB431542 both on neural commitment of hESCs and positional identity of derived neural progenitors in chemically defined substrate-free conditions...
  63. doi request reprint Evidence for abnormal tau phosphorylation in early aggressive multiple sclerosis
    Jane Marian Anderson
    Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Forvie Site, Robinson Way, Cambridge, UK
    Acta Neuropathol 117:583-9. 2009
    ..The absence of sarcosyl-insoluble tau fraction in early disease and its presence in secondary progression raises the possibility that insoluble tau accumulates with disease progression...
  64. ncbi request reprint Making progress on the natural history of multiple sclerosis
    Alastair Compston
    Department of Clinical Neurosciences University of Cambridge Clinical School, Hills Road, Cambridge, UK
    Brain 129:561-3. 2006
  65. ncbi request reprint Oligodendroglial-derived stress signals recruit microglia in vitro
    Richard Nicholas
    University of Cambridge, Neurology Unit, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK
    Neuroreport 14:1001-5. 2003
    ..Thus, whilst the initial recruitment of microglia by stressed oligodendroglia may represent part of a survival process engaged by injured cells, this does not necessarily ensure survival...
  66. ncbi request reprint A scaleable and defined system for generating neural stem cells from human embryonic stem cells
    Alexis J Joannides
    Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, Cambridge, CB2 2PY United Kingdom
    Stem Cells 25:731-7. 2007
    ..This system provides a definitive platform for studying human neural development and has potential therapeutic implications...
  67. ncbi request reprint Revisiting The pathogenesis of multiple sclerosis revisited
    A Compston
    University of Cambridge Neurology Unit, Addenbrooke s Hospital, Cambridge, UK
    Int MS J 10:29-31. 2003
  68. pmc Cognitive presentation of multiple sclerosis: evidence for a cortical variant
    M Zarei
    Department of Neurology, University of Cambridge, Addenbrooke s Hospital, Cambridge, UK
    J Neurol Neurosurg Psychiatry 74:872-7. 2003
    ..Although neuropsychiatric complications are well recognised, the presentation of multiple sclerosis with cognitive or neuropsychiatric symptoms has generally been considered a rare occurrence and to reflect subcortical pathology...
  69. ncbi request reprint Nonactivated microglia promote oligodendrocyte precursor survival and maturation through the transcription factor NF-kappa B
    R S Nicholas
    University of Cambridge Neurology Unit, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 2QQ, UK
    Eur J Neurosci 13:959-67. 2001
    ..These results suggest that, dependent on their state of activation, microglia produce soluble factors that promote oligodendrocyte development through an effect on the PDGF-alpha receptor-signalling pathway...
  70. ncbi request reprint Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis
    A J Coles
    University of Cambridge Neurology Unit, University of Cambridge, UK
    Lancet 354:1691-5. 1999
    ..Multiple sclerosis results from T-cell-dependent inflammatory demyelination of the central nervous system. Our objective was long-term suppression of inflammation with short-term monoclonal antibody treatment...
  71. ncbi request reprint A genome-wide screen for linkage in Nordic sib-pairs with multiple sclerosis
    E Akesson
    University of Cambridge, Neurology Unit, Addenbrooke s Hospital, UK
    Genes Immun 3:279-85. 2002
    ..Our results significantly add to the growing body of linkage data relating to multiple sclerosis...
  72. ncbi request reprint A genome screen for linkage in Australian sibling-pairs with multiple sclerosis
    M Ban
    Neurology Unit, Addenbrooke s Hospital, University of Cambridge, Cambridge, UK
    Genes Immun 3:464-9. 2002
    ..Our results contribute to the available data adding new provisional regions of linkage as well as increasing support for areas previously implicated in genetic susceptibility to multiple sclerosis...
  73. doi request reprint Multiple sclerosis
    Alastair Compston
    Department of Clinical Neurosciences, University of Cambridge Clinical School, Addenbrooke s Hospital, Cambridge, UK
    Lancet 372:1502-17. 2008
    ..We anticipate that future studies in multiple sclerosis will provide a new taxonomy on the basis of mechanisms rather than clinical empiricism, and so inform strategies for improved treatment at all stages of the disease...
  74. ncbi request reprint A genome screen in multiple sclerosis reveals susceptibility loci on chromosome 6p21 and 17q22
    S Sawcer
    University of Cambridge Neurology Unit, Addenbrooke s Hospital, UK
    Nat Genet 13:464-8. 1996
    ..Two principal regions of linkage are identified, chromosomes 17q22 and 6p21 (MHC). Our results are compatible with genetic models involving epistatic interaction between these and several additional genes...
  75. pmc Replication of genome-wide association signals in UK samples reveals risk loci for type 2 diabetes
    Eleftheria Zeggini
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK
    Science 316:1336-41. 2007
    ..The regions identified underscore the importance of pathways influencing pancreatic beta cell development and function in the etiology of type 2 diabetes...
  76. ncbi request reprint A whole genome screen for association in Polish multiple sclerosis patients
    Bartosz Bielecki
    Department of Neurology, Medical University of Lodz, 22 Kopcinskiego Street, 90 153 Lodz, Poland
    J Neuroimmunol 143:107-11. 2003
    ..Five associated markers are identified, one (D6S2444) from the HLA region and four are from novel regions not previously associated with MS, 2p16 (D2S2153), 3p13 (D3S3568), 7p22 (D7S2521) and 15q26 (D15S649)...
  77. ncbi request reprint Two genome-wide linkage disequilibrium screens in Scandinavian multiple sclerosis patients
    Hanne F Harbo
    Institute of Immunology, Rikshospitalet University Hospital, 0027 Oslo, Norway
    J Neuroimmunol 143:101-6. 2003
    ..Usable data were achieved from the same 3331 markers in both screens. Nine markers from eight genomic regions (1p33, 3q13, 6p21, 6q14, 7p22, 9p21, 9q21 and Xq22) were identified as potentially associated with MS in both screens...
  78. ncbi request reprint A whole genome screen for linkage disequilibrium in multiple sclerosis performed in a continental Italian population
    Maria Liguori
    Dipartimento di Scienze Neurologiche e Psichiatriche, Univ Bari, Italy
    J Neuroimmunol 143:97-100. 2003
    ..After refining analysis of the most promising 14 markers to emerge from this screening process, only marker D2S367 retained evidence for association...
  79. ncbi request reprint A genome wide scan for association with multiple sclerosis in a N. Irish case control population
    Shirley Heggarty
    Regional Genetics Service, Belfast City Hospital, Belfast, UK
    J Neuroimmunol 143:93-6. 2003
    ..Putative candidate genes mapping close to the 19 novel markers include the IL10RA and CD3E genes on 11q23 (which both lie close to the marker D11S1998). Individual typing of the marker D11S1998 confirmed its association...
  80. ncbi request reprint A whole genome association study in Icelandic multiple sclerosis patients with 4804 markers
    Aslaug Jonasdottir
    deCODE Genetics, Sturlugata 8, IS 101 Reykjavik, Iceland
    J Neuroimmunol 143:88-92. 2003
    ..Of those, three regions have one or more markers among the 20 most strongly associated: chromosomes 3q25, 6p21.3 (the MHC region) and 19q13...
  81. ncbi request reprint A genome-wide screen for association in Hungarian multiple sclerosis
    Cecilia Rajda
    Department of Neurology, University of Szeged, Semmelweis u 6, H 6725 Szeged, Hungary
    J Neuroimmunol 143:84-7. 2003
    ..These markers were typed in DNA pools that consisted of 88 MS patients (cases), and 128 unrelated controls. Based on a stringent selection criterion, we obtained 33 markers suggesting association with the disease...
  82. ncbi request reprint A genome-wide German screen for linkage disequilibrium in multiple sclerosis
    Alexandra Weber
    Neuroscience Research Center, Institute of Neuroimmunology, Charite University Hospital, 10098 Berlin, Germany
    J Neuroimmunol 143:79-83. 2003
    ..These MHC markers are known to be in linkage disequilibrium with HLA class II alleles influencing susceptibility to MS. The identification of these markers serves as an important positive control...
  83. ncbi request reprint Genetic analysis of multiple sclerosis in Europeans: French data
    Mehdi Alizadeh
    Laboratoire d Immunologie, UPRES EA 1257 IFR97, Faculte de Medecine, 2 Avenue du Pr Léon Bernard CS 34317, 35043 Rennes Cedex, France
    J Neuroimmunol 143:74-8. 2003
    ..These potential associations will require confirmation in further studies...
  84. ncbi request reprint New candidate loci for multiple sclerosis susceptibility revealed by a whole genome association screen in a Belgian population
    An Goris
    Rega Institute for Medical Research, Katholieke Universiteit Leuven, Minderbroedersstraat 10, 3000 Leuven, Belgium
    J Neuroimmunol 143:65-9. 2003
    ..g. the integrin ligand EDIL3, the high-mobility group box protein TOX, neutral sphingomyelinase activating factor (NSMAF) and the B-cell specific transcription factor POU2AF1...
  85. ncbi request reprint A genome screen for linkage disequilibrium in HLA-DRB1*15-positive Germans with multiple sclerosis based on 4666 microsatellite markers
    Rene Goedde
    Department of Molecular Human Genetics, Ruhr University, Universitatsstrasse 150, 44780 Bochum, Germany
    Hum Genet 111:270-7. 2002
    ....
  86. ncbi request reprint A whole genome association study in multiple sclerosis patients from north Portugal
    Berta Martins Silva
    Pathology and Molecular Immunology Department, Instituto Ciências Biomédicas Abel Salazar, University of Porto, Porto, Portugal
    J Neuroimmunol 143:116-9. 2003
    ..When compared to a physical map three regions were found with two of these markers less than 1.5 Mb apart: chromosomes 6p21.3 (the MHC region), 6q14.1 and 7q34...
  87. ncbi request reprint A genomic screen of Spanish multiple sclerosis patients reveals multiple loci associated with the disease
    Robert Goertsches
    Neuroimmunology Unit, Hospital Vall d Hebron, Barcelona, Spain
    J Neuroimmunol 143:124-8. 2003
    ..Our results provide support for the presence of multiple coding regions that contain MS susceptibility genes of small or moderate effect...
  88. ncbi request reprint Evaluating the role of the 620W allele of protein tyrosine phosphatase PTPN22 in Crohn's disease and multiple sclerosis
    Philip L De Jager
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, and Harvard Medical School, Boston, MA 02115, USA
    Eur J Hum Genet 14:317-21. 2006
    ....
  89. ncbi request reprint Multiple sclerosis: light at the end of the tunnel
    Stephen Sawcer
    Eur J Hum Genet 14:257-8. 2006
  90. ncbi request reprint SELPLG and SELP single-nucleotide polymorphisms in multiple sclerosis
    Chiara Fenoglio
    Department of Neurological Sciences, Dino Ferrari Center, University of Milan, IRCCS Ospedale Maggiore Policlinico, Italy
    Neurosci Lett 394:92-6. 2006
    ..Therefore, none of the SNPs investigated is associated with MS, although this analysis does not conclusively exclude SELPLG and SELP as genetic risk factors for MS as much variation remains untested...
  91. ncbi request reprint Ultraconserved regions in multiple sclerosis
    Maria Ban
    Eur J Hum Genet 13:998-9. 2005
  92. pmc Association scan of 14,500 nonsynonymous SNPs in four diseases identifies autoimmunity variants
    Paul R Burton
    Genetic Epidemiology Group, Department of Health Sciences, University of Leicester, Adrian Building, University Road, Leicester LE1 7RH, UK
    Nat Genet 39:1329-37. 2007
    ....
  93. pmc Genetic determinants of ulcerative colitis include the ECM1 locus and five loci implicated in Crohn's disease
    Sheila A Fisher
    Department of Medical and Molecular Genetics, King s College London School of Medicine, 8th Floor Guy s Tower, Guy s Hospital, London SE1 9RT, UK
    Nat Genet 40:710-2. 2008
    ..These data provide the first detailed illustration of the genetic relationship between these common inflammatory bowel diseases...
  94. ncbi request reprint Four single nucleotide polymorphisms from the vitamin D receptor gene in UK multiple sclerosis
    Tai Wai Yeo
    J Neurol 251:753-4. 2004
  95. ncbi request reprint Postnatal astrocytes promote neural induction from adult human bone marrow-derived stem cells
    Alexis Joannides
    Cambridge Centre for Brain Repair and Department of Neurology, University of Cambridge, Cambridge CB2 2PY, UK
    J Hematother Stem Cell Res 12:681-8. 2003
    ..The ability to generate almost limitless numbers of neural precursors from a readily accessible autologous adult human source provides a platform for further studies and potentially has important therapeutic implications...
  96. ncbi request reprint Decreased iNOS synthesis mediates dexamethasone-induced protection of neurons from inflammatory injury in vitro
    Sabine Golde
    Department of Neurology II, Otto von Guericke University, Leipziger Strasse 44, 39120 Magdeburg, Germany
    Eur J Neurosci 18:2527-37. 2003
    ..Our results indicate that the main mechanism of corticosteroid activity on iNOS is reduction in protein synthesis, not destabilization as previously suggested...
  97. ncbi request reprint Risk alleles for multiple sclerosis identified by a genomewide study
    David A Hafler
    Division of Molecular Immunology, Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, and Harvard Medical School, Boston, USA
    N Engl J Med 357:851-62. 2007
    ..Multiple sclerosis has a clinically significant heritable component. We conducted a genomewide association study to identify alleles associated with the risk of multiple sclerosis...