Research Topics
Species | Alasdair J ColesSummaryAffiliation: University of Cambridge Country: UK Publications
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Detail Information
Publications
New treatment strategies in multiple sclerosisJoanne L Jones
Dept of Clinical Neurosciences, Box 165 Addenbrooke s Hospital, Hills Road, Cambridge, CB2 0QQ, UK
Exp Neurol 225:34-9. 2010..In this review, we first sketch the landscape of novel therapies in multiple sclerosis and then discuss in detail approaches which are likely to emerge over the next few years...
Improvement in disability after alemtuzumab treatment of multiple sclerosis is associated with neuroprotective autoimmunityJoanne L Jones
Department of Clinical Neuroscience, University of Cambridge, Addenbrooke s Hospital, Hills Road, Cambridge, CB2 0QQ, UK
Brain 133:2232-47. 2010....
Alemtuzumab versus interferon β-1a in early relapsing-remitting multiple sclerosis: post-hoc and subset analyses of clinical efficacy outcomesAlasdair J Coles
Department of Neurosciences, University of Cambridge, Addenbrooke s Hospital, Cambridge, UK
Lancet Neurol 10:338-48. 2011..Additionally, we aimed to describe a new outcome measure in multiple sclerosis research: sustained reduction in disability...
Alemtuzumab therapy for multiple sclerosisAlasdair J Coles
Department of Clinical Neurosciences, University of Cambridge, Addenbrooke s Hospital, Cambridge, CB2 0QQ, UK
Neurotherapeutics 10:29-33. 2013..Its use requires careful monitoring so that potentially serious side effects can be treated early and effectively...
Alemtuzumab for patients with relapsing multiple sclerosis after disease-modifying therapy: a randomised controlled phase 3 trialAlasdair J Coles
Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
Lancet 380:1829-39. 2012..We aimed to assess efficacy and safety of alemtuzumab compared with interferon beta 1a in patients who have relapsed despite first-line treatment...
Alemtuzumab more effective than interferon β-1a at 5-year follow-up of CAMMS223 clinical trialA J Coles
Department of Neurosciences, University of Cambridge, Addenbrooke s Hospital, Cambridge UK
Neurology 78:1069-78. 2012....
Campath-1H treatment of multiple sclerosis: lessons from the bedside for the benchAlasdair Coles
Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 2QQ, UK
Clin Neurol Neurosurg 106:270-4. 2004
Unilateral calf hypertrophyA Coles
Department of Neurology, Box 165, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK
J Neurol Neurosurg Psychiatry 75:1606. 2004
The window of therapeutic opportunity in multiple sclerosis: evidence from monoclonal antibody therapyAlasdair J Coles
Department of Clinical Neurosciences, Box 165, Addenbrooke s Hospital, Cambridge CB2 2QQ, UK
J Neurol 253:98-108. 2006..These concepts are currently being tested in a controlled trial comparing Campath-1H and IFN-beta in the treatment of drug-naïve patients with early, active RR MS...
Dehydroepiandrosterone replacement in patients with Addison's disease has a bimodal effect on regulatory (CD4+CD25hi and CD4+FoxP3+) T cellsAlasdair J Coles
Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
Eur J Immunol 35:3694-703. 2005....
B-cell reconstitution and BAFF after alemtuzumab (Campath-1H) treatment of multiple sclerosisSara A J Thompson
Department of Clinical Neurosciences, University of Cambridge, Addenbrooke s Hospital, Cambridge, UK
J Clin Immunol 30:99-105. 2010..Differentiation to memory B cells is slow so there are radical and prolonged alterations to the B-cell pool after alemtuzumab...
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...
Lymphocyte homeostasis following therapeutic lymphocyte depletion in multiple sclerosisAmanda L Cox
Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
Eur J Immunol 35:3332-42. 2005..We speculate that CCL21 and IL-15 responses to lymphopaenia may be suboptimal in multiple sclerosis...
Campath-1H treatment of multiple sclerosisJoanne L Jones
Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
Neurodegener Dis 5:27-31. 2008..Here, we summarise our clinical and laboratory findings, describing how this prototypical 'bench to bedside' therapy continues to inform basic science, revealing aspects of the pathogenesis of multiple sclerosis and autoimmunity...
Long term lymphocyte reconstitution after alemtuzumab treatment of multiple sclerosisGrant A Hill-Cawthorne
Department of Neurology, University of Cambridge, Cambridge, UK
J Neurol Neurosurg Psychiatry 83:298-304. 2012..The long term effects on lymphocyte reconstitution of a single course, and the consequences that this has on disability, morbidity, mortality and autoimmunity, were examined...
Notes on the kidney and its diseases for the neurologistMichael S Zandi
Department of Clinical Neurosciences, University of Cambridge, Box 165, Addenbrooke s Hospital, Cambridge, UK
J Neurol Neurosurg Psychiatry 78:444-9. 2007..We consider the current evolving trial evidence that directs the usage of a growing arsenal of therapies in the induction and maintenance stages of vasculitis treatment, and extend this consideration to Lupus and Sjogren's...
No association between multiple sclerosis and the Notch3 gene responsible for cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)S A Broadley
University of Cambridge Neurology Unit, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 2QQ, UK
J Neurol Neurosurg Psychiatry 71:97-9. 2001..No evidence for association was found in any of the three markers and none of the commoner mutations causing CADASIL were found in the sequenced patients...
