Imperial College London

DrRichardNicholas

Faculty of MedicineDepartment of Brain Sciences

Professor of Practice (Neurology)
 
 
 
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r.nicholas

 
 
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12L12CLab BlockCharing Cross Campus

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Publications

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232 results found

Datta G, Violante IR, Scott G, Zimmerman K, Santos-Ribeiro A, Rabiner EA, Gunn RN, Malik O, Ciccarelli O, Nicholas R, Matthews PMet al., 2016, Translocator positron-emission tomography and magnetic resonance spectroscopic imaging of brain glial cell activation in multiple sclerosis., Multiple Sclerosis, Vol: 23, Pages: 1469-1478, ISSN: 1352-4585

BACKGROUND: Multiple sclerosis (MS) is characterised by a diffuse inflammatory response mediated by microglia and astrocytes. Brain translocator protein (TSPO) positron-emission tomography (PET) and [myo-inositol] magnetic resonance spectroscopy (MRS) were used together to assess this. OBJECTIVE: To explore the in vivo relationships between MRS and PET [(11)C]PBR28 in MS over a range of brain inflammatory burden. METHODS: A total of 23 patients were studied. TSPO PET imaging with [(11)C]PBR28, single voxel MRS and conventional magnetic resonance imaging (MRI) sequences were undertaken. Disability was assessed by Expanded Disability Status Scale (EDSS) and Multiple Sclerosis Functional Composite (MSFC). RESULTS: [(11)C]PBR28 uptake and [ myo-inositol] were not associated. When the whole cohort was stratified by higher [(11)C]PBR28 inflammatory burden, [ myo-inositol] was positively correlated to [(11)C]PBR28 uptake (Spearman's ρ = 0.685, p = 0.014). Moderate correlations were found between [(11)C]PBR28 uptake and both MRS creatine normalised N-acetyl aspartate (NAA) concentration and grey matter volume. MSFC was correlated with grey matter volume (ρ = 0.535, p = 0.009). There were no associations between other imaging or clinical measures. CONCLUSION: MRS [ myo-inositol] and PET [(11)C]PBR28 measure independent inflammatory processes which may be more commonly found together with more severe inflammatory disease. Microglial activation measured by [(11)C]PBR28 uptake was associated with loss of neuronal integrity and grey matter atrophy.

Journal article

Lewin A, Hamilton S, Witkover A, Langford P, Nicholas R, Chataway J, Bangham CRet al., 2016, Free serum haemoglobin is associated with brain atrophy in secondary progressive multiple sclerosis [version 1; peer review: 1 approved, 2 approved with reservations], Wellcome Open Research, Vol: 1, ISSN: 2398-502X

Background A major cause of disability in secondary progressive multiple sclerosis (SPMS) is progressive brain atrophy, whose pathogenesis is not fully understood. The objective of this study was to identify protein biomarkers of brain atrophy in SPMS. Methods We used surface-enhanced laser desorption-ionization time-of-flight mass spectrometry to carry out an unbiased search for serum proteins whose concentration correlated with the rate of brain atrophy, measured by serial MRI scans over a 2-year period in a well-characterized cohort of 140 patients with SPMS. Protein species were identified by liquid chromatography-electrospray ionization tandem mass spectrometry. Results There was a significant (p<0.004) correlation between the rate of brain atrophy and a rise in the concentration of proteins at 15.1 kDa and 15.9 kDa in the serum. Tandem mass spectrometry identified these proteins as alpha-haemoglobin and beta-haemoglobin, respectively.  The abnormal concentration of free serum haemoglobin was confirmed by ELISA (p<0.001). The serum lactate dehydrogenase activity was also highly significantly raised (p<10(-12)) in patients with secondary progressive multiple sclerosis. Conclusions An underlying low-grade chronic intravascular haemolysis is a potential source of the iron whose deposition along blood vessels in multiple sclerosis plaques contributes to the neurodegeneration and consequent brain atrophy seen in progressive disease. Chelators of free serum iron will be ineffective in preventing this neurodegeneration, because the iron (Fe(2+)) is chelated by haemoglobin.

Journal article

Newbould R, Muraro P, Bishop C, Waldman Aet al., 2016, Analysis of ageing-associated grey matter volume in patients with multiple sclerosis shows excess atrophy in subcortical regions, NeuroImage-Clinical, Vol: 13, Pages: 9-15, ISSN: 2213-1582

Age of onset in multiple sclerosis (MS) exerts an influence on the course of disease. This study examined whether global and regional brain volumes differed between “younger” and “older” onset MS subjects who were matched for short disease duration, mean 1.9 years and burden as measured by the MS Severity Score and relapses.21 younger-onset MS subjects (age 30.4 ± 3.2 years) were compared with 17 older-onset (age 48.7 ± 3.3 years) as well as age-matched controls (n = 31, 31.9 ± 3.5 years and n = 21, 47.3 ± 4.0 years). All subjects underwent 3D volumetric T1 and T2-FLAIR imaging. White matter (WM) and grey matter (GM) lesions were outlined manually. Lesions were filled prior to tissue and structural segmentation to reduce classification errors.Volume loss versus control was predominantly in the subcortical GM, at > 13% loss. Younger and older-onset MS subjects had similar, strong excess loss in the putamen, thalamus, and nucleus accumbens. No excess loss was detected in the amygdala or pallidum. The hippocampus and caudate showed significant excess loss in the younger group (p < 0.001) and a strong trend in the older-onset group.These results provide a potential imaging correlate of published neuropsychological studies that reported the association of younger age at disease onset with impaired cognitive performance, including decreased working memory.

Journal article

Bermel R, Comi G, Eralinna J-P, Leist TP, Nicholas R, Oreja-Guevara C, Siva A, Van Wijmeersch B, Wiendl H, Bernasconi C, Buffels R, Csoboth C, Han J, Musch B, Vermersch Pet al., 2016, Design of two phase III open-label trials evaluating ocrelizumab in patients with relapsing-remitting multiple sclerosis and suboptimal response to disease-modifying treatment, 32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE PUBLICATIONS LTD, Pages: 615-616, ISSN: 1352-4585

Conference paper

Gafson AR, Nicholas R, Giovannoni G, Matthews PMet al., 2016, Plasma cytokine concentration changes in multiple sclerosis patients after treatment with dimethyl fumarate, 32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE PUBLICATIONS LTD, Pages: 670-671, ISSN: 1352-4585

Conference paper

Chan D, Binks S, Nicholas J, Frost C, Alsanousi A, Fox N, Wilkie D, Nicholas R, Chataway Jet al., 2016, Effect of high-dose simvastatin on cognition in secondary progressive multiple sclerosis (MS-STAT cognitive): a randomised, placebo-controlled, Phase 2 trial., 32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE PUBLICATIONS LTD, Pages: 82-83, ISSN: 1352-4585

Conference paper

Datta G, Colasanti A, Kalk NJ, Owen DR, Scott G, Rabiner EA, Gunn RN, Lingford-Hughes AR, Malik O, Ciccarelli O, Nicholas R, Battaglini M, Stefano ND, Matthews PMet al., 2016, In vivo translocator protein positron emission tomography imaging detects a heterogeneity of lesion inflammatory activity in multiple sclerosis not evident by MRI., 32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE PUBLICATIONS LTD, Pages: 36-37, ISSN: 1352-4585

Conference paper

Mitchell B, Raffel J, Nicholas R, 2016, Increasing area level deprivation in England impacts age of progression and wheelchair use in multiple sclerosis, 32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE PUBLICATIONS LTD, Pages: 503-503, ISSN: 1352-4585

Conference paper

Connell L, Daws R, Hampshire A, Nicholas R, Raffel Jet al., 2016, Validating a participant-led computerised cognitive battery in people with multiple sclerosis, 32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE PUBLICATIONS LTD, Pages: 140-141, ISSN: 1352-4585

Conference paper

Wallace A, Raffel J, Reynolds R, Friede T, Nicholas Ret al., 2016, Increased multiple sclerosis impact scale-29 score is associated with reduced survival in multiple sclerosis, 32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE PUBLICATIONS LTD, Pages: 455-456, ISSN: 1352-4585

Conference paper

Record C, De Simoni S, Feeney C, Sharp D, Nicholas R, Raffel Jet al., 2016, Improved cerebral blood flow after natalizumab treatment in multiple sclerosis, 32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE Publications, Pages: 669-669, ISSN: 1352-4585

Conference paper

Peress L, Violante IR, Scott G, Zimmerman K, Sharp D, Nicholas R, Raffel Jet al., 2016, Thalamic magnetic resonance spectroscopy in highly active multiple sclerosis, 32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE PUBLICATIONS LTD, Pages: 210-211, ISSN: 1352-4585

Conference paper

Dorsey-Campbell RJ, Quinn T, Felongco T, Delacruz D, Walters P, Scalfari A, Singh-Curry V, Malik O, Nicholas Ret al., 2016, Pharmacy-led monitoring of disease modifying treatments in multiple sclerosis improves the quality of monitoring and improves patient satisfaction, 32nd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE PUBLICATIONS LTD, Pages: 792-792, ISSN: 1352-4585

Conference paper

Dubis AM, Nandoskar A, Kalitzeos A, Patel PJ, Carroll J, Dubra A, Chataway J, Nicholas R, Michaelides M, Greenwood Jet al., 2016, Retinal Vessel Architecture and Blood Flow in Multiple Sclerosis, Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology (ARVO), Publisher: ASSOC RESEARCH VISION OPHTHALMOLOGY INC, ISSN: 0146-0404

Conference paper

Lema A, Bishop C, Malik O, Mattoscio M, Ali R, Nicholas R, Muraro PA, Matthews PM, Waldman AD, Newbould RDet al., 2016, A compararison of magnetization transfer methods to assess brain and cervical cord microstructure in multiple sclerosis, Journal of Neuroimaging, Vol: 27, Pages: 221-226, ISSN: 1552-6569

BACKGROUND: Demyelination is a core pathological feature of multiple sclerosis (MS) and spontaneous remyelination appears to be an important mechanism for repair in the disease. Magnetization transfer ratio imaging (MTR) has been used extensively to evaluate demyelination, although limitations to its specificity are recognized. MT saturation imaging (MTsat) removes some of the T1 dependence of MTR. We have performed a comparative evaluation of MTR and MTsat imaging in a mixed group of subjects with active MS, to explore their relative sensitivity to pathology relevant to explaining clinical outcomes. METHODS: A total of 134 subjects underwent MRI of their brain and cervical spinal cord. Isotropic 3-dimensional pre- and postcontrast T1-weighted and T2-weighted fluid-attenuated inversion recovery (FLAIR) volumes were segmented into brain normal appearing white matter (NAWM), brain WM lesions (WML), normal appearing spinal cord (NASC), and spinal cord lesions. Volumes and metrics for MTR and MTsat histograms were calculated for each region. RESULTS: Significant Spearman correlations were found with the Expanded Disability Status Scale and timed 25-foot walk for the whole brain and WML MTR, but not in that from the NAWM or any cervical spinal cord region. By contrast, the MTsat was correlated with both disability metrics in all these regions in both the brain and spine. CONCLUSIONS: This study extends prior work relating atrophy and lesion load with disability, by characterization of MTsat parameters. MTsat is practical in routine clinical applications and may be more sensitive to tissue damage than MTR for both brain and cervical spinal cord.

Journal article

Cruz PMR, Matthews L, Boggild M, Cavey A, Constantinescu CS, Evangelou N, Giovannoni G, Gray O, Hawkins S, Nicholas R, Oppenheimer M, Robertson N, Zajicek J, Rothwell PM, Palace Jet al., 2016, Time- and Region-Specific Season of Birth Effects in Multiple Sclerosis in the United Kingdom, JAMA NEUROLOGY, Vol: 73, Pages: 954-960, ISSN: 2168-6149

Journal article

Martin J, Raffel JB, Nicholas R, 2016, Progressive Dwindling in Multiple Sclerosis: An Opportunity to Improve Care, PLOS One, Vol: 11, ISSN: 1932-6203

IntroductionIn the general ageing population, 40% of deaths occur following a prolonged trajectory of “progressive dwindling,” characterised by chronic accumulation of disability and frailty, and associated with increased dependency and reduced reserves. Those who progressively dwindle are poorly catered for by current healthcare systems and would benefit from a coordinated approach to their medical and social care, known as formative care. People with multiple sclerosis (pwMS) may be more likely to progressively dwindle, and may be appropriate targets for formative care pathways.ObjectivesTo determine the proportion of pwMS who follow a progressive dwindling trajectory prior to death. To relate trajectory to place of death, and examine what factors predict the progressively dwindling trajectory.MethodsA retrospective observational study of 582 deceased pwMS enrolled in the UK MS Tissue Bank, including death certificates and extensive clinical summaries.Results73.7% of pwMS had a “progressively dwindling” trajectory of dying. This was predicted by those who reach MS disease milestones earlier. 72.5% of pwMS died an MS-related death, which was predicted by an aggressive disease course from onset. Those who progressively dwindled were equally likely to die in hospital as those with other trajectories to death.ConclusionsThe progressively dwindling trajectory of dying is very common in pwMS, and can be predicted by earlier disease milestones. Pathways could target pwMS in these years prior to death, to improve care.

Journal article

Colasanti A, Guo Q, Giannetti P, Wall M, Newbould R, Bishop C, Onega M, Nicholas R, Ciccarelli O, Muraro P, Malik O, Owen D, Young A, Gunn R, Piccini P, Matthews P, Rabiner Eet al., 2016, Neuroinflammation and genesis of affective symptoms in multiple sclerosis: integrating evidence from TSPO PET and resting state FMRI, Bipolar Disorders, Vol: 18, Pages: 84-84, ISSN: 1398-5647

Journal article

Feeney C, Scott G, Raffel J, Roberts S, Coello C, Jolly A, Searle G, Goldstone AP, Brooks DJ, Nicholas RS, Trigg W, Gunn RN, Sharp DJet al., 2016, Kinetic analysis of the translocator protein positron emission tomography ligand [18F]GE-180 in the human brain, European Journal of Nuclear Medicine and Molecular Imaging, Vol: 43, Pages: 2201-2210, ISSN: 1619-7089

PURPOSE: PET can image neuroinflammation by targeting the translocator protein (TSPO), which is upregulated in activated microglia. The high nonspecific binding of the first-generation TSPO radioligand [(11)C]PK-11195 limits accurate quantification. [(18)F]GE-180, a novel TSPO ligand, displays superior binding to [(11)C]PK-11195 in vitro. Our objectives were to: (1) evaluate tracer characteristics of [(18)F]GE-180 in the brains of healthy human subjects; and (2) investigate whether the TSPO Ala147Thr polymorphism influences outcome measures. METHODS: Ten volunteers (five high-affinity binders, HABs, and five mixed-affinity binders, MABs) underwent a dynamic PET scan with arterial sampling after injection of [(18)F]GE-180. Kinetic modelling of time-activity curves with one-tissue and two-tissue compartment models and Logan graphical analysis was applied to the data. The primary outcome measure was the total volume of distribution (V T) across various regions of interest (ROIs). Secondary outcome measures were the standardized uptake values (SUV), the distribution volume and SUV ratios estimated using a pseudoreference region. RESULTS: The two-tissue compartment model was the best model. The average regional delivery rate constant (K 1) was 0.01 mL cm(-3) min(-1) indicating low extraction across the blood-brain barrier (1 %). The estimated median V T across all ROIs was also low, ranging from 0.16 mL cm(-3) in the striatum to 0.38 mL cm(-3) in the thalamus. There were no significant differences in V T between HABs and MABs across all ROIs. CONCLUSION: A reversible two-tissue compartment model fitted the data well and determined that the tracer has a low first-pass extraction (approximately 1 %) and low V T estimates in healthy individuals. There was no observable dependency on the rs6971 polymorphism as compared to other second-generation TSPO PET tracers. Investigation of [(18)F]GE-180 in populations with neuroinflammatory disease is nee

Journal article

Macdonell R, Nagels G, Laplaud D-A, Pozzilli C, de Jong B, da Silva AM, Nicholas R, Lechner-Scott J, Gaebler JA, Agarwal S, Wang P, Yeh M, Hovenden M, Sorensen PSet al., 2016, Improved patient-reported health impact of multiple sclerosis: The ENABLE study of PR-fampridine, MULTIPLE SCLEROSIS JOURNAL, Vol: 22, Pages: 944-954, ISSN: 1352-4585

Journal article

Nicotra A, Newman C, Johnson M, Eremin O, Friede T, Malik O, Nicholas Ret al., 2016, Peripheral nerve dysfunction in middle-aged subjects born with thalidomide embryopathy, PLOS One, Vol: 11, ISSN: 1932-6203

BackgroundPhocomelia is an extremely rare congenital malformation that emerged as one extreme of arange of defects resulting from in utero exposure to thalidomide. Individuals with thalidomideembryopathy (TE) have reported developing symptoms suggestive of peripheral nervoussystem dysfunction in the mal-developed limbs in later life.MethodsCase control study comparing TE subjects with upper limb anomalies and neuropathicsymptoms with healthy controls using standard neurophysiological testing. Other causes ofa peripheral neuropathy were excluded prior to assessment.ResultsClinical examination of 17 subjects with TE (aged 50.4±1.3 [mean±standard deviation]years, 10 females) and 17 controls (37.9±9.0 years; 8 females) demonstrated features ofupper limb compressive neuropathy in three-quarters of subjects. Additionally there wereexamination findings suggestive of mild sensory neuropathy in the lower limbs (n = 1), L5radiculopathic sensory impairment (n = 1) and cervical myelopathy (n = 1). In TE there wereelectrophysiological changes consistent with a median large fibre neuropathic abnormality(mean compound muscle action potential difference -6.3 mV ([-9.3, -3.3], p = 0.0002) ([95%CI], p-value)) and reduced sympathetic skin response amplitudes (-0.8 mV ([-1.5, -0.2], p =0.0089)) in the affected upper limbs. In the lower limbs there was evidence of sural nervedysfunction (sensory nerve action potential -5.8 μV ([-10.7, -0.8], p = 0.0232)) and impairedwarm perception thresholds (+3.0°C ([0.6, 5.4], p = 0.0169)).ConclusionsWe found a range of clinical features relevant to individuals with TE beyond upper limb compressiveneuropathies supporting the need for a detailed neurological examination toexclude other treatable pathologies. The electrophysiological evidence of large and smallfibre axonal nerve dysfunction in symptomatic and asymptomatic limbs may be a result ofthe original insult and merits further investigation.

Journal article

de Paula Alves Sousa A, Johnson KR, Nicholas R, Darko S, Price DA, Douek DC, Jacobson S, Muraro PAet al., 2016, Intrathecal T-cell clonal expansions in patients with multiple sclerosis, Annals of Clinical and Translational Neurology, Vol: 3, Pages: 422-433, ISSN: 2328-9503

ObjectiveAnalysis of the T-cell receptor (TCR) repertoire in the cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS) can reveal antigen-specific immune responses potentially implicated in the disease process. We applied a new unbiased deep-sequencing method for TCR repertoire analysis to accurately measure and compare receptor diversity and clonal expansions within the peripheral and CSF-trafficking T-cell populations of patients with MS and control individuals with idiopathic intracranial hypertension (IIH).MethodsPaired blood and CSF TCR β-chain libraries from five MS patients and five IIH controls were sequenced, yielding a total of 80 million reads.ResultsAlthough TCR repertoire diversity was greater in the blood and CSF compartments of MS patients when compared with IIH controls, it is notable that the frequency of clonal expansions was also significantly higher in both compartments of MS patients. Highly expanded T-cell clones were enriched in the CSF compartment of MS patients compared to peripheral blood, very few of them were detected in both compartments.InterpretationCollectively, our data provide a proof of principle that private compartmentalized T-cell expansion exists in the intrathecal space of MS patients.

Journal article

Porter J, Arie G, Nicholas R, Matthews Pet al., 2016, Transcriptome Profiles from Relapsing-Remitting Multiple Sclerosis Patients Show Aberrant Immunological Phenotypes Compared with Healthy Controls, 68th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878

Conference paper

Datta G, Battaglini M, Scott G, Yaldizli O, Santos-Ribeiro A, Rabiner E, Gunn R, Owen D, Malik O, Ciccarelli O, Nicholas R, Langdon D, De Stefano N, Matthews Pet al., 2016, Cortical [11C]PBR28 PET Measures of Microglial Inflammation Explain Differences in Cognitive Performance of People with MS, 68th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878

Conference paper

Porter J, Arie G, Nicholas R, Matthews Pet al., 2016, Transcriptome Profiles from Relapsing-Remitting Multiple Sclerosis Patients Show Aberrant Immunological Phenotypes Compared with Healthy Controls, 68th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878

Conference paper

Datta G, Battaglini M, Scott G, Yaldizli O, Santos-Ribeiro A, Rabiner E, Gunn R, Owen D, Malik O, Ciccarelli O, Nicholas R, Langdon D, De Stefano N, Matthews Pet al., 2016, Cortical [11C]PBR28 PET Measures of Microglial Inflammation Explain Differences in Cognitive Performance of People with MS, 68th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878

Conference paper

Datta G, Battaglini M, Scott G, Yaldizli O, Santos-Ribeiro A, Rabiner E, Gunn R, Owen D, Malik O, Ciccarelli O, Nicholas R, Langdon D, De Stefano N, Matthews Pet al., 2016, Cortical [11C]PBR28 PET Measures of Microglial Inflammation Explain Differences in Cognitive Performance of People with MS, 68th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878

Conference paper

Datta G, Battaglini M, Scott G, Yaldizli O, Santos-Ribeiro A, Rabiner E, Gunn R, Owen D, Malik O, Ciccarelli O, Nicholas R, Langdon D, De Stefano N, Matthews Pet al., 2016, Cortical [11C]PBR28 PET Measures of Microglial Inflammation Explain Differences in Cognitive Performance of People with MS, 68th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878

Conference paper

Datta G, Battaglini M, Scott G, Yaldizli O, Santos-Ribeiro A, Rabiner E, Gunn R, Owen D, Malik O, Ciccarelli O, Nicholas R, Langdon D, De Stefano N, Matthews Pet al., 2016, Cortical [11C]PBR28 PET Measures of Microglial Inflammation Explain Differences in Cognitive Performance of People with MS, 68th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878

Conference paper

Datta G, Battaglini M, Scott G, Yaldizli O, Santos-Ribeiro A, Rabiner E, Gunn R, Owen D, Malik O, Ciccarelli O, Nicholas R, Langdon D, De Stefano N, Matthews Pet al., 2016, Cortical [11C]PBR28 PET Measures of Microglial Inflammation Explain Differences in Cognitive Performance of People with MS, 68th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878

Conference paper

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