Publications
225 results found
Nicholas R, Rashid W, 2013, Multiple sclerosis., Am Fam Physician, Vol: 87, Pages: 712-714
Ali R, Nicholas RSJ, Muraro PA, 2013, Drugs in Development for Relapsing Multiple Sclerosis, DRUGS, Vol: 73, Pages: 625-650, ISSN: 0012-6667
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- Citations: 38
Howell O, Schulz-Trieglaff EK, Carassiti D, et al., 2013, Grey matter pathology in the cerebellum in multiple sclerosis is linked to inflammation in the subarachnoid space, 114th Meeting of the British-Neuropathological-Society / Symposium on Advances in Motor Neuron Diseases, Publisher: WILEY-BLACKWELL, Pages: 19-20, ISSN: 0305-1846
Giannetti P, Politis M, Su P, et al., 2013, Microglia Activation in Clinically Isolated Syndrome: 11C11195PK-PET Change within Normal Appearing White Matter and Deep Grey Matter Structures, 65th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878
Politis M, Giannetti P, Niccolini F, et al., 2013, Decreased Microglial Activation Precedes Stabilization of Disability in Multiple Sclerosis Patients Treated with Natalizumab, 65th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878
Chataway J, Schuerer N, Alsanousi A, et al., 2013, THE MS-STAT TRIAL: High Dose Simvastatin Slows Brain Atrophy and Delays Disability in Secondary Progressive Multiple Sclerosis: A Phase II Placebo-Controlled Trial, 65th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878
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- Citations: 4
Mattoscio M, Nicholas R, Malik O, et al., 2013, Circulating Hematopoietic Stem Cell Numbers during Natalizumab Treatment in Patients with Multiple Sclerosis: Association with Clinical and MRI Variables, 65th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878
Nicholas R, Dahdaleh D, Altmann DM, et al., 2013, Authors' reply, The Lancet, Vol: 381, Pages: 201-202, ISSN: 0140-6736
Durrenberger PF, Webb LV, Sim MJ, et al., 2012, Increased HLA-E expression in white matter lesions in multiple sclerosis., Immunology, Vol: 137, Pages: 317-325, ISSN: 0019-2805
AbstractThe molecular mechanisms underpinning central nervous system (CNS) damage in multiple sclerosis (MS) are complex and it is widely accepted that there is an autoimmune component. Both adaptive and innate immune effector mechanisms are believed to contribute to tissue disease aetiology. HLA-E is a non-classical MHC class Ib molecule that acts as the ligand for the NKG2A inhibitory receptor present on natural killer (NK) and CD8(+) cells. Peptide binding and stabilisation of HLA-E is often considered to signal infection or cell stress. Here we examine the up-regulation of HLA-E in MS brain tissue. Expression is significantly increased in white matter lesions in the brain of MS patients compared to white matter of neurologically healthy controls. Furthermore, using quantitative immunohistochemistry and confocal microscopy, we show increased HLA-E protein expression in endothelial cells of active MS lesions. Non-inflammatory chronic lesions express significantly less HLA-E protein, comparable to levels found in white matter from controls. Increased HLA-E protein levels were associated with higher scores of inflammation. These results suggest the potential for an effect in CNS pathogenesis from HLA-E modulation in stressed tissue. Co-localisation with infiltrating CD8(+) cells implicates a possible role for HLA-E restricted regulatory CD8(+) cells, as has been proposed in other autoimmune diseases.
Choi SR, Howell OW, Carassiti D, et al., 2012, Meningeal inflammation plays a role in the pathology of primary progressive multiple sclerosis, BRAIN, Vol: 135, Pages: 2925-2937, ISSN: 0006-8950
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- Citations: 158
Chataway J, Alsanousi A, Chan D, et al., 2012, The MS-STAT trial: high dose simvastatin demonstrates neuroprotection without immune-modulation in secondary progressive multiple sclerosis (SPMS) - a phase II trial, 28th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis, Publisher: SAGE PUBLICATIONS LTD, Pages: 509-509, ISSN: 1352-4585
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- Citations: 6
Reynolds R, Howell O, Choi S, et al., 2012, Meningeal inflammation and cortical pathology play a prominent role in primary progressive multiple sclerosis, 28th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis, Publisher: SAGE PUBLICATIONS LTD, Pages: 119-120, ISSN: 1352-4585
Magliozzi R, Arico E, Durrenberger P, et al., 2012, Gene expression profiling of cortical lesions in secondary progressive multiple sclerosis, 28th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis, Publisher: SAGE PUBLICATIONS LTD, Pages: 121-121, ISSN: 1352-4585
Howell OW, Nicholas R, Gveric D, et al., 2012, THE RISK OF SEIZURES IN PROGRESSIVE MULTIPLE SCLEROSIS, 10th European Congress on Epileptology, Publisher: WILEY-BLACKWELL, Pages: 24-25, ISSN: 0013-9580
Nicholas R, Straube S, Schmidli H, et al., 2012, Time-patterns of annualized relapse rates in randomized placebo-controlled clinical trials in relapsing multiple sclerosis: A systematic review and meta-analysis, MULTIPLE SCLEROSIS JOURNAL, Vol: 18, Pages: 1290-1296, ISSN: 1352-4585
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- Citations: 17
Chataway J, Alsanousi A, Chan D, et al., 2012, The MS-STAT trial: a randomised placebo-controlled phase II trial of high dose simvastatin in secondary progressive multiple sclerosis (SPMS), 16th Congress of the European-Federation-of-Neurological-Societies (EFNS), Publisher: WILEY-BLACKWELL, Pages: 87-87, ISSN: 1351-5101
Dahdaleh D, Altmann DM, Malik O, et al., 2012, Breathlessness, night sweats, and weight loss on natalizumab, LANCET, Vol: 380, Pages: 726-727, ISSN: 0140-6736
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- Citations: 13
Politis M, Giannetti P, Su P, et al., 2012, Increased PK11195 PET binding in the cortex of patients with MS correlates with disability, NEUROLOGY, Vol: 79, Pages: 523-530, ISSN: 0028-3878
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- Citations: 97
Parsons N, Friede T, Todd S, et al., 2012, An R package for implementing simulations for seamless phase II/III clinical trials using early outcomes for treatment selection, COMPUTATIONAL STATISTICS & DATA ANALYSIS, Vol: 56, Pages: 1150-1160, ISSN: 0167-9473
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- Citations: 5
Mattoscio M, Nicholas R, Malik O, et al., 2012, Differential Increase of Circulating Haematopoietic Stem Cells (HSC) Following Therapeutic alpha 4-Integrin Blockade in Multiple Sclerosis: Correlation between HSC Mobilization Status and Response to Treatment, 64th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878
Mattoscio M, Nicholas R, Malik O, et al., 2012, Differential Increase of Circulating Haematopoietic Stem Cells (HSC) Following Therapeutic alpha 4-Integrin Blockade in Multiple Sclerosis: Correlation between HSC Mobilization Status and Response to Treatment, 64th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878
Nicholas R, Rashid W, 2012, Multiple sclerosis., BMJ Clin Evid, Vol: 2012
INTRODUCTION: Multiple sclerosis is the most common cause of neurological disability in young adults. Irreversible disability can occur, but life expectancy is generally not affected. METHODS AND OUTCOMES: We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of interventions aimed at reducing relapse rates and disability in people with multiple sclerosis? What are the effects of interventions to improve symptoms during acute relapse? What are the effects of treatments for fatigue, spasticity, and multidisciplinary care on disability in people with multiple sclerosis? We searched: Medline, Embase, The Cochrane Library, and other important databases up to July 2011 (Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA). RESULTS: We found 71 systematic reviews, RCTs, and observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions. CONCLUSIONS: In this systematic review, we present information relating to the effectiveness and safety of the following key interventions: amantadine, azathioprine, behaviour modification, botulinum toxin, corticosteroids, exercise, gabapentin, inpatient or outpatient rehabilitation, interferon beta, intrathecal baclofen, intravenous immunoglobulin, methotrexate, mitoxantrone, modafinil, natalizumab, oral drug treatments, parenteral glatiramer acetate, physiotherapy, and plasma exchange.
Durrenberger PF, Ettorre A, Kamel F, et al., 2012, Innate Immunity in multiple sclerosis white matter lesions: expression of natural cytotoxicity triggering receptor 1 (NCR1), Journal of Neuroinflammation, Vol: 9, ISSN: 1742-2094
Giannetti P, Politis M, Su P, et al., 2012, PK11195-PET Enhancement in Black Holes Correlates with Disability and Outcome in Progressive Multiple Sclerosis, 137th Annual Meeting of the American-Neurological-Association (ANA), Publisher: WILEY-BLACKWELL, Pages: S112-S112, ISSN: 0364-5134
Giannetti P, Niccolini F, Nicholas R, 2012, BG-12 and its potential for the prevention of relapse in multiple sclerosis., Degener Neurol Neuromuscul Dis, Vol: 2, Pages: 119-132
Multiple sclerosis (MS) arises from an immune attack on the central nervous system producing demyelination and axonal loss. Clinically the relapsing-remitting course is characterized by subacute onset of neurological symptoms usually with partial or complete recovery, while the progressive course, predominant in the later stages, is characterized by progressive disability in the absence of relapses. A number of disease-modifying treatments have been developed and are increasingly effective at targeting relapses. Early injectable therapies such as interferon and glatiramer acetate are only partially effective, but have a good safety record. Recently, natalizumab, an intravenous therapy, demonstrated increased effectiveness, but side effects complicate its use. The first oral therapy offering good efficacy and convenience, fingolimod, was approved in USA in 2010 and Europe in 2011. BG-12 is a potential novel oral therapy for MS, which has previously been used as a different formulation for psoriasis. It has anti-inflammatory and neuroprotective actions in vitro, which makes it a promising candidate for future therapies. Phase II studies showed that BG-12 reduced MRI inflammatory activity over placebo, which was confirmed in two Phase III studies indicating immune modulation may be its principal action rather than neuroprotection. In these studies, BG-12 reduced relapse rates consistently with variable effects on progression and few serious adverse events. With its favorable efficacy-tolerability profile, BG-12 could offer a substantial step forward for the care for subjects affected by relapsing MS.
Thapar A, Lane TRA, Nicholas R, 2012, Chronic Cerebrospinal Venous Insufficiency: It is an entity and a subset of multiple sclerosis - Against The Motion, Vascular and Endovascular Controversies Update, Editors: Greenhalgh, Publisher: BIBA Medical, Pages: 696-705
Ettorre A, Kamel FO, Durrenberger PF, et al., 2011, KIR expression as a biomarker of multiple sclerosis disease type, Annual Congress of the British-Society-for-Immunology, Publisher: WILEY-BLACKWELL, Pages: 172-172, ISSN: 0019-2805
Kamel F, Ettorre A, Durrenberger PF, et al., 2011, Altered invariant natural killer T cells in multiple sclerosis, Annual Congress of the British-Society-for-Immunology, Publisher: WILEY-BLACKWELL, Pages: 41-41, ISSN: 0019-2805
Thapar A, Lane T, Nicholas R, et al., 2011, Systematic review of sonographic chronic cerebrospinal venous insufficiency findings in multiple sclerosis, PHLEBOLOGY, Vol: 26, Pages: 319-325, ISSN: 0268-3555
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- Citations: 8
Nicholas R, Straube S, Schmidli H, et al., 2011, Trends in annualized relapse rates in relapsing-remitting multiple sclerosis and consequences for clinical trial design, MULTIPLE SCLEROSIS JOURNAL, Vol: 17, Pages: 1211-1217, ISSN: 1352-4585
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- Citations: 31
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