Imperial College London

Professor Paul M. Matthews

Faculty of MedicineDepartment of Brain Sciences

Edmond and Lily Safra Chair. Head of Department
 
 
 
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Contact

 

+44 (0)20 7594 2855p.matthews

 
 
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Assistant

 

Ms Siobhan Dillon +44 (0)20 7594 2855

 
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Location

 

E502Burlington DanesHammersmith Campus

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Summary

 

Publications

Publication Type
Year
to

599 results found

Tzimopoulou S, Cunningham VJ, Nichols TE, Searle G, Bird NP, Mistry P, Dixon IJ, Hallett WA, Whitcher B, Brown AP, Zvartau-Hind M, Lotay N, Lai RYK, Castiglia M, Jeter B, Matthews JC, Chen K, Bandy D, Reiman EM, Gold M, Rabiner EA, Matthews PMet al., 2011, Validation and pilot application of [ <sup>18</sup>F]FDG-PET in evaluation of a metabolic therapy for Alzheimer's disease, Advances in Alzheimer's Disease, Vol: 2, Pages: 627-642, ISSN: 2210-5727

Here we describe methods for application of quantitative fluorodeoxyglucose positron emission tomography ([ 18F]FDG-PET) measures of brain glucose metabolism in multi-centre clinical trials for Alzheimer's disease. We validated methods and demonstrated their use in the context of a treatment trial with the PPARγ agonist Rosiglitazone XR versus placebo in mild to moderate AD patients. Novel quantitative indices related to the combined forward rate constant for [ 18F]FDG uptake \(({K}-{i}^{index})\) and to the rate of cerebral glucose utilization \((CM{R}-{glu}^{index})\) were applied. Active treatment was associated with a sustained but not statistically significant trend from the first month for higher mean values in both. However, neither these nor another analytical approach recently validated using data from the Alzheimer's Disease Neuroimaging Initiative suggested that active treatment decreased the progression of decline in brain glucose metabolism. Rates of brain atrophy were similar between active and placebo groups and measures of cognition also did not demonstrate clear group differences. Our study demonstrates the feasibility of using [ 18F]FDG-PET as part of a multi-centre therapeutics trial and describes new measures that can be employed. It suggests that Rosiglitazone is associated with an early increase in whole brain glucose utilisation, but not with any biological or clinical evidence for slowing progression over the period of study in the selected patient group. © 2011 The authors and IOS Press. All rights reserved.

Journal article

Patsopoulos NA, de Bakker PIW, 2011, Genome-wide meta-analysis identifies novel multiple sclerosis susceptibility loci, ANNALS OF NEUROLOGY, Vol: 70, Pages: 897-912, ISSN: 0364-5134

Journal article

Narayanan S, Caramanos Z, Matthews PM, Arnold DLet al., 2011, Axonal pathology in patients with multiple sclerosis: Evidence from in vivo proton magnetic resonance spectroscopy, Multiple Sclerosis Therapeutics, Fourth Edition, Pages: 150-164, ISBN: 9780521766272

© Cambridge University Press 2011. Introduction The clinical course of multiple sclerosis (MS) is highly variable, and pathological changes that are seen with the disease are heterogeneous amongst individuals. In recent years, there has been increasing interest in the development of magnetic resonance imaging (MRI) approaches to characterizing the pathological substrates of disability in MS with the objective of developing quantitative in vivo indices of pathology that could provide new insights into the pathogenesis of the disease, as well as provide more specific or sensitive end-points for treatment trials. This chapter reviews results from studies that have used either proton magnetic resonance spectroscopy (1H-MRS, a technique that allows for the acquisition of 1H-MR spectra from single voxels) or 1H-MR spectroscopic imaging (1H-MRSI, a technique that allows for the simultaneous acquisition of 1H-MR spectra from multiple voxels) to measure in vivo chemical pathology associated with impairment of axonal metabolic or structural integrity, and places these results in the context of relevant histopathological investigations. We will focus on an important hypothesis that has developed from these studies: that axonal pathology is central to the final common pathway leading to the progressive disability that is seen in individuals with this disease.

Book chapter

De Silva A, Salem V, Long CJ, Makwana A, Newbould RD, Rabiner EA, Ghatei MA, Bloom SR, Matthews PM, Beaver JD, Dhillo WSet al., 2011, The Gut Hormones PYY3-36 and GLP-1(7-36) amide Reduce Food Intake and Modulate Brain Activity in Appetite Centers in Humans, CELL METABOLISM, Vol: 14, Pages: 700-706, ISSN: 1550-4131

Journal article

Thomas EL, Makwana A, Newbould R, Rao AW, Gambarota G, Frost G, Delafont B, Mishra RG, Matthews PM, Berk ES, Schwartz SM, Bell JD, Beaver JDet al., 2011, Pragmatic study of orlistat 60mg on abdominal obesity, EUROPEAN JOURNAL OF CLINICAL NUTRITION, Vol: 65, Pages: 1256-1262, ISSN: 0954-3007

Journal article

Strijbis EMM, Inkster B, Vounou M, Kappos L, Radu E-W, Matthews PM, Uitdehaag B, Barkhof F, Geurts JJGet al., 2011, The explanatory value of glutamatergic SNPs on combined MRI phenotypes in multiple sclerosis, MULTIPLE SCLEROSIS JOURNAL, Vol: 17, Pages: S114-S115, ISSN: 1352-4585

Journal article

Inkster B, Strijbis EMM, Vounou M, Kappos L, Radue EW, Matthews PM, Uitdehaag B, Barkhof F, Polman CH, Montana G, Geurts JJGet al., 2011, Mitochondrial sirtuin gene variants and brain volume changes in patients with multiple sclerosis, MULTIPLE SCLEROSIS JOURNAL, Vol: 17, Pages: S333-S334, ISSN: 1352-4585

Journal article

Matthews PM, Rabiner I, Gunn R, 2011, Non-invasive imaging in experimental medicine for drug development, CURRENT OPINION IN PHARMACOLOGY, Vol: 11, Pages: 501-507, ISSN: 1471-4892

Journal article

Inkster B, Rao AW, Ridler K, Nichols TE, Saemann PG, Auer DP, Holsboer F, Tozzi F, Muglia P, Merlo-Pich E, Matthews PMet al., 2011, Structural Brain Changes in Patients with Recurrent Major Depressive Disorder Presenting with Anxiety Symptoms, JOURNAL OF NEUROIMAGING, Vol: 21, Pages: 375-382, ISSN: 1051-2284

Journal article

Bosnell RA, Kincses T, Stagg CJ, Tomassini V, Kischka U, Jbabdi S, Woolrich MW, Andersson J, Matthews PM, Johansen-Berg Het al., 2011, Motor Practice Promotes Increased Activity in Brain Regions Structurally Disconnected After Subcortical Stroke, NEUROREHABILITATION AND NEURAL REPAIR, Vol: 25, Pages: 607-616, ISSN: 1545-9683

Journal article

Roosendaal SD, Bendfeldt K, Vrenken H, Polman CH, Borgwardt S, Radue EW, Kappos L, Pelletier D, Hauser SL, Matthews PM, Barkhof F, Geurts JJGet al., 2011, Grey matter volume in a large cohort of MS patients: relation to MRI parameters and disability, MULTIPLE SCLEROSIS JOURNAL, Vol: 17, Pages: 1098-1106, ISSN: 1352-4585

Journal article

Colasanti A, Searle GE, Long CJ, Hill SP, Reiley RR, Tziortzi AC, Quelch D, Gunn R, Waldman AD, Schruers KJ, Matthews PM, Nutt DJ, Rabiner EAet al., 2011, OPIOID RELEASE IN HUMAN BRAIN REWARD SYSTEM INDUCED BY AN ACUTE AMPHETAMINE CHALLENGE: A [11C]CARFENTANIL PET STUDY, Summer Meeting of the British-Association-for-Psychopharmacology, Publisher: SAGE PUBLICATIONS LTD, Pages: A60-A60, ISSN: 0269-8811

Conference paper

Beaver JD, Long CJ, Cole DM, Durcan MJ, Bannon LC, Mishra RG, Matthews PMet al., 2011, The Effects of Nicotine Replacement on Cognitive Brain Activity During Smoking Withdrawal Studied with Simultaneous fMRI/EEG, NEUROPSYCHOPHARMACOLOGY, Vol: 36, Pages: 1792-1800, ISSN: 0893-133X

Journal article

Rabiner EA, Beaver J, Makwana A, Searle G, Long C, Nathan PJ, Newbould RD, Howard J, Miller SR, Bush MA, Hill S, Reiley R, Passchier J, Gunn RN, Matthews PM, Bullmore ETet al., 2011, Molecular and functional neuroimaging of human opioid receptor pharmacology., Mol Psychiatry, Vol: 16

Journal article

Dixson L, Ridler K, Nichols TE, Saemann PG, Auer DP, Holsboer F, Muglia P, Matthews PM, Inkster Bet al., 2011, Thyroid hormone transporter genes and grey matter changes in patients with major depressive disorder and healthy controls, PSYCHONEUROENDOCRINOLOGY, Vol: 36, Pages: 929-934, ISSN: 0306-4530

Journal article

Sombekke MH, Jafari N, Bendfeldt K, Mueller-Lenke N, Radue EW, Naegelin Y, Kappos L, Matthews PM, Polman CH, Barkhof F, Hintzen R, Geurts JJGet al., 2011, NO INFLUENCE OF KIF1B ON NEURODEGENERATIVE MARKERS IN MULTIPLE SCLEROSIS, NEUROLOGY, Vol: 76, Pages: 1843-1845, ISSN: 0028-3878

Journal article

James A, Hough M, James S, Winmill L, Burge L, Nijhawan S, Matthews PM, Zarei Met al., 2011, Greater white and grey matter changes associated with early cannabis use in adolescent-onset schizophrenia (AOS), SCHIZOPHRENIA RESEARCH, Vol: 128, Pages: 91-97, ISSN: 0920-9964

Journal article

Stagg CJ, Jayaram G, Pastor D, Kincses ZT, Matthews PM, Johansen-Berg Het al., 2011, Polarity and timing-dependent effects of transcranial direct current stimulation in explicit motor learning, NEUROPSYCHOLOGIA, Vol: 49, Pages: 800-804, ISSN: 0028-3932

Journal article

Douaud G, Jbabdi S, Behrens TEJ, Menke RA, Gass A, Monsch AU, Rao A, Whitcher B, Kindlmann G, Matthews PM, Smith Set al., 2011, DTI measures in crossing-fibre areas: Increased diffusion anisotropy reveals early white matter alteration in MCI and mild Alzheimer's disease, NEUROIMAGE, Vol: 55, Pages: 880-890, ISSN: 1053-8119

Journal article

Dennis A, Bosnell R, Dawes H, Howells K, Cockburn J, Kischka U, Matthews P, Johansen-Berg Het al., 2011, Cognitive Context Determines Dorsal Premotor Cortical Activity During Hand Movement in Patients After Stroke, STROKE, Vol: 42, Pages: 1056-1061, ISSN: 0039-2499

Journal article

Valsasina P, Rocca MA, Absinta M, Sormani MP, Mancini L, De Stefano N, Rovira A, Gass A, Enzinger C, Barkhof F, Wegner C, Matthews PM, Filippi Met al., 2011, A multicentre study of motor functional connectivity changes in patients with multiple sclerosis, EUROPEAN JOURNAL OF NEUROSCIENCE, Vol: 33, Pages: 1256-1263, ISSN: 0953-816X

Journal article

Tomassini V, Jbabdi S, Kincses ZT, Bosnell R, Douaud G, Pozzilli C, Matthews PM, Johansen-Berg Het al., 2011, Structural and Functional Bases for Individual Differences in Motor Learning, HUMAN BRAIN MAPPING, Vol: 32, Pages: 494-508, ISSN: 1065-9471

Journal article

Owen DRJ, Piccini P, Matthews PM, 2011, Towards molecular imaging of multiple sclerosis, MULTIPLE SCLEROSIS JOURNAL, Vol: 17, Pages: 262-272, ISSN: 1352-4585

Journal article

Bush WS, McCauley JL, DeJager PL, Dudek SM, Hafler DA, Gibson RA, Matthews PM, Kappos L, Naegelin Y, Polman CH, Hauser SL, Oksenberg J, Haines JL, Ritchie MDet al., 2011, A knowledge-driven interaction analysis reveals potential neurodegenerative mechanism of multiple sclerosis susceptibility, Genes and Immunity, Vol: 12, Pages: 335-340, ISSN: 1466-4879

Gene–gene interactions are proposed as an important component of the genetic architecture of complex diseases, and are just beginning to be evaluated in the context of genome-wide association studies (GWAS). In addition to detecting epistasis, a benefit to interaction analysis is that it also increases power to detect weak main effects. We conducted a knowledge-driven interaction analysis of a GWAS of 931 multiple sclerosis (MS) trios to discover gene–gene interactions within established biological contexts. We identify heterogeneous signals, including a gene–gene interaction between CHRM3 (muscarinic cholinergic receptor 3) and MYLK (myosin light-chain kinase) (joint P=0.0002), an interaction between two phospholipase C-β isoforms, PLCβ1 and PLCβ4 (joint P=0.0098), and a modest interaction between ACTN1 (actinin alpha 1) and MYH9 (myosin heavy chain 9) (joint P=0.0326), all localized to calcium-signaled cytoskeletal regulation. Furthermore, we discover a main effect (joint P=5.2E−5) previously unidentified by single-locus analysis within another related gene, SCIN (scinderin), a calcium-binding cytoskeleton regulatory protein. This work illustrates that knowledge-driven interaction analysis of GWAS data is a feasible approach to identify new genetic effects. The results of this study are among the first gene–gene interactions and non-immune susceptibility loci for MS. Further, the implicated genes cluster within inter-related biological mechanisms that suggest a neurodegenerative component to MS.

Journal article

James A, Hough M, James S, Burge L, Winmill L, Nijhawan S, Matthews PM, Zarei Met al., 2011, Structural brain and neuropsychometric changes associated with pediatric bipolar disorder with psychosis, BIPOLAR DISORDERS, Vol: 13, Pages: 16-27, ISSN: 1398-5647

Journal article

Wang JH, Pappas D, De Jager PL, Pelletier D, de Bakker PIW, Kappos L, Polman CH, Chibnik LB, Hafler DA, Matthews PM, Hauser SL, Baranzini SE, Oksenberg JRet al., 2011, Modeling the cumulative genetic risk for multiple sclerosis from genome-wide association data, GENOME MEDICINE, Vol: 3, ISSN: 1756-994X

Background:Multiple sclerosis (MS) is the most common cause of chronic neurologic disability beginning in early tomiddle adult life. Results from recent genome-wide association studies (GWAS) have substantially lengthened the list ofdisease loci and provide convincing evidence supporting a multifactorial and polygenic model of inheritance.Nevertheless, the knowledge of MS genetics remains incomplete, with many risk alleles still to be revealed.Methods:We used a discovery GWAS dataset (8,844 samples, 2,124 cases and 6,720 controls) and a multi-step logisticregression protocol to identify novel genetic associations. The emerging genetic profile included 350 independentmarkers and was used to calculate and estimate the cumulative genetic risk in an independent validation dataset (3,606samples). Analysis of covariance (ANCOVA) was implemented to compare clinical characteristics of individuals withvarious degrees of genetic risk. Gene ontology and pathway enrichment analysis was done using the DAVID functionalannotation tool, the GO Tree Machine, and the Pathway-Express profiling tool.Results:In the discovery dataset, the median cumulative genetic risk (P-Hat) was 0.903 and 0.007 in the case andcontrol groups, respectively, together with 79.9% classification sensitivity and 95.8% specificity. The identified profileshows a significant enrichment of genes involved in the immune response, cell adhesion, cell communication/signaling, nervous system development, and neuronal signaling, including ionotropic glutamate receptors, whichhave been implicated in the pathological mechanism driving neurodegeneration. In the validation dataset, themedian cumulative genetic risk was 0.59 and 0.32 in the case and control groups, respectively, with classificationsensitivity 62.3% and specificity 75.9%. No differences in disease progression or T2-lesion volumes were observedamong four levels of predicted genetic risk groups (high, medium, low, misclassified). On the other hand, asignifican

Journal article

Owen DRJ, Matthews PM, 2011, IMAGING BRAIN MICROGLIAL ACTIVATION USING POSITRON EMISSION TOMOGRAPHY AND TRANSLOCATOR PROTEIN-SPECIFIC RADIOLIGANDS, BIOMARKERS OF NEUROLOGICAL AND PSYCHIATRIC DISEASE, Vol: 101, Pages: 19-39, ISSN: 0074-7742

Journal article

Crofts JJ, Higham DJ, Bosnell R, Jbabdi S, Matthews PM, Behrens TEJ, Johansen-Berg Het al., 2011, Network analysis detects changes in the contralesional hemisphere following stroke, NEUROIMAGE, Vol: 54, Pages: 161-169, ISSN: 1053-8119

Journal article

Tomassini V, Johansen-Berg H, Leonardi L, Paixao L, Jbabdi S, Palace J, Pozzilli C, Matthews PMet al., 2011, Preservation of motor skill learning in patients with multiple sclerosis, MULTIPLE SCLEROSIS JOURNAL, Vol: 17, Pages: 103-115, ISSN: 1352-4585

Journal article

Filippini N, Ebmeier KP, MacIntosh BJ, Trachtenberg AJ, Frisoni GB, Wilcock GK, Beckmann CF, Smith SM, Matthews PM, Mackay CEet al., 2011, Differential effects of the APOE genotype on brain function across the lifespan, NEUROIMAGE, Vol: 54, Pages: 602-610, ISSN: 1053-8119

Journal article

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