Publications
757 results found
Baranzini SE, Srinivasan R, Khankhanian P, et al., 2010, Genetic variation influences glutamate concentrations in brains of patients with multiple sclerosis, BRAIN, Vol: 133, Pages: 2603-2611, ISSN: 0006-8950
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- Citations: 96
Cole DM, Beckmann CF, Long CJ, et al., 2010, Nicotine replacement in abstinent smokers improves cognitive withdrawal symptoms with modulation of resting brain network dynamics, NEUROIMAGE, Vol: 52, Pages: 590-599, ISSN: 1053-8119
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- Citations: 144
Beaver JD, Bullmore ET, Searle GE, et al., 2010, Differentiation of the Mu-opioid ligand GSK1521498 from naltrexone using [11C]carfentanil PET and fMRI, 8th International Symposium on Functional Neuroreceptor Mapping of the Living Brain, Publisher: ACADEMIC PRESS INC ELSEVIER SCIENCE, Pages: S78-S78, ISSN: 1053-8119
Owen DR, Rabiner EA, Gunn RN, et al., 2010, PBR28, PBR06 and PBR111 bind two distinct TSPO sites in human brain tissue, 8th International Symposium on Functional Neuroreceptor Mapping of the Living Brain, Publisher: ACADEMIC PRESS INC ELSEVIER SCIENCE, Pages: S30-S31, ISSN: 1053-8119
Kasperaviciute D, Catarino CB, Heinzen EL, et al., 2010, Common genetic variation and susceptibility to partial epilepsies: a genome-wide association study, Brain, Vol: 133, Pages: 2136-2147, ISSN: 1460-2156
Partial epilepsies have a substantial heritability. However, the actual genetic causes are largely unknown. In contrast to many other common diseases for which genetic association-studies have successfully revealed common variants associated with disease risk, the role of common variation in partial epilepsies has not yet been explored in a well-powered study. We undertook a genome-wide association-study to identify common variants which influence risk for epilepsy shared amongst partial epilepsy syndromes, in 3445 patients and 6935 controls of European ancestry. We did not identify any genome-wide significant association. A few single nucleotide polymorphisms may warrant further investigation. We exclude common genetic variants with effect sizes above a modest 1.3 odds ratio for a single variant as contributors to genetic susceptibility shared across the partial epilepsies. We show that, at best, common genetic variation can only have a modest role in predisposition to the partial epilepsies when considered across syndromes in Europeans. The genetic architecture of the partial epilepsies is likely to be very complex, reflecting genotypic and phenotypic heterogeneity. Larger meta-analyses are required to identify variants of smaller effect sizes (odds ratio <1.3) or syndrome-specific variants. Further, our results suggest research efforts should also be directed towards identifying the multiple rare variants likely to account for at least part of the heritability of the partial epilepsies. Data emerging from genome-wide association-studies will be valuable during the next serious challenge of interpreting all the genetic variation emerging from whole-genome sequencing studies.
Zarei M, Patenaude B, Damoiseaux J, et al., 2010, Combining shape and connectivity analysis: An MRI study of thalamic degeneration in Alzheimer's disease (vol 49, pg 1, 2010), NEUROIMAGE, Vol: 51, Pages: 940-940, ISSN: 1053-8119
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- Citations: 1
Heinzen EL, Radtke RA, Urban TJ, et al., 2010, Rare Deletions at 16p13.11 Predispose to a Diverse Spectrum of Sporadic Epilepsy Syndromes, AMERICAN JOURNAL OF HUMAN GENETICS, Vol: 86, Pages: 707-718, ISSN: 0002-9297
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- Citations: 201
Pomeroy IM, Jordan EK, Frank JA, et al., 2010, Focal and diffuse cortical degenerative changes in a marmoset model of multiple sclerosis, MULTIPLE SCLEROSIS JOURNAL, Vol: 16, Pages: 537-548, ISSN: 1352-4585
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- Citations: 23
Matthews PM, 2010, IMAGING FOR TRANSLATIONAL PHARMACOLOGY, IRISH JOURNAL OF MEDICAL SCIENCE, Vol: 179, Pages: S99-S100, ISSN: 0021-1265
Giorgio A, Watkins KE, Chadwick M, et al., 2010, Longitudinal changes in grey and white matter during adolescence, NEUROIMAGE, Vol: 49, Pages: 94-103, ISSN: 1053-8119
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- Citations: 293
Zarei M, Patenaude B, Damoiseaux J, et al., 2010, Combining shape and connectivity analysis: An MRI study of thalamic degeneration in Alzheimer's disease, NEUROIMAGE, Vol: 49, Pages: 1-8, ISSN: 1053-8119
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- Citations: 133
Tzimopoulou S, Cunningham VJ, Nichols TE, et al., 2010, A Multi-Center Randomized Proof-of-Concept Clinical Trial Applying [<SUP>18</SUP>F]FDG-PET for Evaluation of Metabolic Therapy with Rosiglitazone XR in Mild to Moderate Alzheimer's Disease, JOURNAL OF ALZHEIMERS DISEASE, Vol: 22, Pages: 1241-1256, ISSN: 1387-2877
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- Citations: 81
Antoniades A, Matthews PM, Pattichis CS, et al., 2010, A Computationally Fast Measure Of Epistasis For 2 SNPs And A Categorical Phenotype, 2010 ANNUAL INTERNATIONAL CONFERENCE OF THE IEEE ENGINEERING IN MEDICINE AND BIOLOGY SOCIETY (EMBC), Pages: 6194-6197, ISSN: 1557-170X
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- Citations: 3
Owen DR, Howell OW, Tang SP, et al., 2010, Two binding sites for [3H]PBR28 in human brain: implications for TSPO PET imaging of neuroinflammation, J Cereb Blood Flow Metab, Vol: 30, Pages: 1608-1618, ISSN: 1559-7016
[(11)C]PBR28, a radioligand targeting the translocator protein (TSPO), does not produce a specific binding signal in approximately 14% of healthy volunteers. This phenomenon has not been reported for [(11)C]PK11195, another TSPO radioligand. We measured the specific binding signals with [(3)H]PK11195 and [(3)H]PBR28 in brain tissue from 22 donors. Overall, 23% of the samples did not generate a visually detectable specific autoradiographic signal with [(3)H]PBR28, although all samples showed [(3)H]PK11195 binding. There was a marked reduction in the affinity of [(3)H]PBR28 for TSPO in samples with no visible [(3)H]PBR28 autoradiographic signal (K(i)=188+/-15.6 nmol/L), relative to those showing normal signal (K(i)=3.4+/-0.5 nmol/L, P<0.001). Of this latter group, [(3)H]PBR28 bound with a two-site fit in 40% of cases, with affinities (K(i)) of 4.0+/-2.4 nmol/L (high-affinity site) and 313+/-77 nmol/L (low-affinity site). There was no difference in K(d) or B(max) for [(3)H]PK11195 in samples showing no [(3)H]PBR28 autoradiographic signal relative to those showing normal [(3)H]PBR28 autoradiographic signal. [(3)H]PK11195 bound with a single site for all samples. The existence of three different binding patterns with PBR28 (high-affinity binding (46%), low-affinity binding (23%), and two-site binding (31%)) suggests that a reduction in [(11)C]PBR28 binding may not be interpreted simply as a reduction in TSPO density. The functional significance of differences in binding characteristics warrants further investigation.
Matthews P, 2010, Library and information management at the University of the West of England, ASLIB PROCEEDINGS, Vol: 62, Pages: 537-538, ISSN: 0001-253X
Matthews P, Anderson S, 2010, CINEMA, SUBJECTIVITY AND PSYCHOSIS: TOWARDS A PHENOMENOLOGICAL APPROACH, Publisher: ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER, ISSN: 0924-9338
Nalbantian S, Matthews PM, McClelland JL, 2010, The Memory Process, Publisher: Mit Pr, ISBN: 9780262014571
The convergence of neuroscience, philosophy, art, music, and literature offers valuablenew insights into the study of memory.
Voets NL, Adcock JE, Stacey R, et al., 2009, Functional and Structural Changes in the Memory Network Associated with Left Temporal Lobe Epilepsy, HUMAN BRAIN MAPPING, Vol: 30, Pages: 4070-4081, ISSN: 1065-9471
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- Citations: 63
Matthews PM, Comley R, 2009, Advances in the molecular imaging of multiple sclerosis, EXPERT REVIEW OF CLINICAL IMMUNOLOGY, Vol: 5, Pages: 765-777, ISSN: 1744-666X
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- Citations: 7
Tomassini V, Johansen-Berg H, Leonardi L, et al., 2009, MOTOR SKILL LEARNING IN MULTIPLE SCLEROSIS, Joint Annual Meeting of the Association-of-British-Neurologists/Spanish-Society-of-Neurology, Publisher: BMJ PUBLISHING GROUP, ISSN: 0022-3050
Stagg CJ, O'Shea J, Kincses ZT, et al., 2009, Modulation of movement-associated cortical activation by transcranial direct current stimulation, EUROPEAN JOURNAL OF NEUROSCIENCE, Vol: 30, Pages: 1412-1423, ISSN: 0953-816X
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- Citations: 127
Zarei M, Menke RA, Scholz J, et al., 2009, Multimodal MR imaging of substantia nigra in Parkinson's disease, 19th World Congress of Neurology, Publisher: ELSEVIER SCIENCE BV, Pages: S293-S293, ISSN: 0022-510X
Douaud G, Mackay C, Andersson J, et al., 2009, Schizophrenia delays and alters maturation of the brain in adolescence, BRAIN, Vol: 132, Pages: 2437-2448, ISSN: 0006-8950
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- Citations: 114
Menke RA, Scholz J, Miller KL, et al., 2009, MRI characteristics of the substantia nigra in Parkinson's disease: A combined quantitative T1 and DTI study, NEUROIMAGE, Vol: 47, Pages: 435-441, ISSN: 1053-8119
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- Citations: 131
Stefansson H, Ophoff RA, Steinberg S, et al., 2009, Common variants conferring risk of schizophrenia, NATURE, Vol: 460, Pages: 744-U99, ISSN: 0028-0836
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- Citations: 1262
Cader S, Palace J, Matthews PM, 2009, Cholinergic agonism alters cognitive processing and enhances brain functional connectivity in patients with multiple sclerosis, JOURNAL OF PSYCHOPHARMACOLOGY, Vol: 23, Pages: 686-696, ISSN: 0269-8811
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- Citations: 31
Rocca MA, Absinta M, Valsasina P, et al., 2009, Abnormal Connectivity of the Sensorimotor Network in Patients With MS: A MultiCenter fMRI Study, HUMAN BRAIN MAPPING, Vol: 30, Pages: 2412-2425, ISSN: 1065-9471
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- Citations: 45
Inkster B, Nichols TE, Saemann PG, et al., 2009, Association of <i>GSK</i>3β Polymorphisms With Brain Structural Changes in Major Depressive Disorder, ARCHIVES OF GENERAL PSYCHIATRY, Vol: 66, Pages: 721-728, ISSN: 0003-990X
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- Citations: 83
De Jager PL, Jia X, Wang J, et al., 2009, Meta-analysis of genome scans and replication identify <i>CD6</i>, <i>IRF8</i> and <i>TNFRSF1A</i> as new multiple sclerosis susceptibility loci, NATURE GENETICS, Vol: 41, Pages: 776-U26, ISSN: 1061-4036
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- Citations: 618
Enzinger C, Dawes H, Johansen-Berg H, et al., 2009, Brain Activity Changes Associated With Treadmill Training After Stroke, STROKE, Vol: 40, Pages: 2460-2467, ISSN: 0039-2499
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- Citations: 110
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