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Jenna Price

Bio: Jenna Price is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Type 2 diabetes & Journalism. The author has an hindex of 9, co-authored 23 publications receiving 1194 citations. Previous affiliations of Jenna Price include University of Technology, Sydney & Australian National University.

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Journal ArticleDOI
Daniel I. Swerdlow1, Michael V. Holmes1, Karoline Kuchenbaecker2, Engmann Jel.1, Tina Shah1, Reecha Sofat1, Yiran Guo, C Chung1, Anne Peasey1, Roman Pfister3, Simon P. Mooijaart4, Helen Ireland1, Maarten Leusink5, Claudia Langenberg3, KaWah Li1, Jutta Palmen1, Phil Howard1, Jackie A. Cooper1, Fotios Drenos1, John Hardy1, Mike A. Nalls6, Yun Li7, Gordon D.O. Lowe8, Marlene C. W. Stewart9, S. J. Bielinski10, Julian Peto11, Nicholas J. Timpson12, John Gallacher13, Malcolm G. Dunlop9, Richard S. Houlston, Ian Tomlinson14, Ioanna Tzoulaki15, Jian'an Luan2, Boer Jma.2, Nita G. Forouhi2, N. C. Onland-Moret5, Y. T. van der Schouw16, Renate B. Schnabel16, Jaroslav A. Hubacek, Růžena Kubínová, Migle Baceviciene17, Abdonas Tamosiunas17, Andrzej Pajak18, Roman Topor-Madry18, Sofia Malyutina19, Damiano Baldassarre, Bengt Sennblad20, Elena Tremoli, U de Faire21, Luigi Ferrucci21, S Bandenelli, Tetsu Tanaka21, James F. Meschia10, AB Singleton6, Gerjan Navis22, I. Mateo Leach22, Bakker Sjl.22, Ron T. Gansevoort, Ian Ford8, Stephen E. Epstein23, Mary-Susan Burnett23, Joe Devaney23, Johan Wouter Jukema4, Westendorp Rgj.5, G Jan de Borst5, Y. van der Graaf5, P A de Jong5, Mailand-van der Zee A-H.5, Olaf H. Klungel5, A. de Boer5, P. A. Doevendans5, Jeffrey W. Stephens24, Charles B. Eaton25, Jennifer G. Robinson26, JoAnn E. Manson27, F G Fowkes28, Timothy M. Frayling28, Jenna Price9, Peter H. Whincup11, Richard W Morris1, Debbie A Lawlor12, George Davey Smith12, Yoav Ben-Shlomo12, Susan Redline27, Leslie A. Lange29, Meena Kumari1, Nicholas J. Wareham2, Verschuren Wmm.30, Emelia J. Benjamin30, John C. Whittaker11, Anders Hamsten20, Frank Dudbridge11, Delaney Jac.31, Andrew Wong31, Diana Kuh31, Rebecca Hardy31, Berta Almoguera Castillo7, John Connolly7, P. van der Harst, Eric J. Brunner1, Michael Marmot1, Christina L. Wassel32, Steve E. Humphries1, P.J. Talmud1, Mika Kivimäki1, Folkert W. Asselbergs5, Mikhail I. Voevoda19, Martin Bobak1, Hynek Pikhart1, James G. Wilson33, Hakon Hakonarson7, Alexander P. Reiner34, Brendan J. Keating7, Naveed Sattar8, Aroon D. Hingorani1, Juan P. Casas11 
TL;DR: IL6R blockade could provide a novel therapeutic approach to prevention of coronary heart disease that warrants testing in suitably powered randomised trials and could help to validate and prioritise novel drug targets or to repurpose existing agents and targets for new therapeutic uses.

891 citations

Journal ArticleDOI
Carla A. Ibrahim-Verbaas1, Jan Bressler2, Stéphanie Debette, Maaike Schuur1, Albert V. Smith3, J. C. Bis4, Gary Davies5, Stella Trompet6, Jennifer A. Smith7, Christiane Wolf8, Lori B. Chibnik9, Yongmei Liu10, Veronique Vitart5, Mirna Kirin5, Katja Petrovic11, Ozren Polasek12, Lina Zgaga13, Chloe Fawns-Ritchie5, Peter Hoffmann14, Peter Hoffmann15, Juha Karjalainen16, Jari Lahti17, David J. Llewellyn18, Carsten Oliver Schmidt19, Karen A. Mather20, Vincent Chouraki21, Qi Sun9, Susan M. Resnick22, Lynda M. Rose9, Christopher Oldmeadow23, Marlene C. W. Stewart5, Blair H. Smith24, Vilmundur Gudnason3, Qiong Yang25, Saira Saeed Mirza1, Johan Wouter Jukema6, P. L. DeJager9, T.B. Harris22, D C Liewald5, Najaf Amin1, Laura H. Coker10, Oliver Stegle8, Oscar L. Lopez26, Reinhold Schmidt11, Alexander Teumer19, Ian Ford27, Nazanin Karbalai8, James T. Becker26, Maria K. Jonsdottir, Rhoda Au22, Rudolf S N Fehrmann16, Stefan Herms15, Stefan Herms14, Mike A. Nalls22, Wei Zhao7, Stephen T. Turner28, Kristine Yaffe29, Kurt Lohman10, J. C. van Swieten1, Sharon L.R. Kardia7, D. S. Knopman28, William M. Meeks30, Gerardo Heiss31, Elizabeth G. Holliday23, Peter W. Schofield23, Toshiko Tanaka22, David J. Stott27, Jing Wang25, Paul M. Ridker9, Alan J. Gow5, Alison Pattie5, John M. Starr5, Lynne J. Hocking32, Nicola J. Armstrong20, Stela McLachlan5, Joshua M. Shulman33, Luke C. Pilling18, G. Eiriksdottir, Rodney J. Scott23, Nicole A. Kochan20, Aarno Palotie17, Y. C. Hsieh34, Johan G. Eriksson, Alan D. Penman30, Rebecca F. Gottesman35, Ben A. Oostra1, Le Yu36, Anita L. DeStefano25, Alexa S. Beiser25, Melissa Garcia22, Jerome I. Rotter37, Jerome I. Rotter38, Markus M. Nöthen39, Albert Hofman1, P.E. Slagboom6, R.G.J. Westendorp, Brendan M. Buckley40, Philip A. Wolf22, André G. Uitterlinden1, Bruce M. Psaty41, Hans-Jörgen Grabe19, Stefania Bandinelli, Daniel I. Chasman9, Francine Grodstein9, Katri Räikkönen17, Jean-Charles Lambert21, David J. Porteous5, Jenna Price5, Perminder S. Sachdev20, Luigi Ferrucci22, John Attia23, Igor Rudan5, Caroline Hayward5, Alan F. Wright5, James F. Wilson5, Sven Cichon, Lude Franke16, Helena Schmidt11, Jun Ding10, A.J.M. de Craen6, Myriam Fornage2, David A. Bennett36, Ian J. Deary5, M. A. Ikram1, L. J. Launer22, Annette L. Fitzpatrick4, Sudha Seshadri22, C M van Duijn1, Thomas H. Mosley30 
TL;DR: This article conducted a GWAS of executive functioning and information processing speed in non-demented older adults from the CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) consortium.
Abstract: To identify common variants contributing to normal variation in two specific domains of cognitive functioning, we conducted a genome-wide association study (GWAS) of executive functioning and information processing speed in non-demented older adults from the CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) consortium. Neuropsychological testing was available for 5429-32,070 subjects of European ancestry aged 45 years or older, free of dementia and clinical stroke at the time of cognitive testing from 20 cohorts in the discovery phase. We analyzed performance on the Trail Making Test parts A and B, the Letter Digit Substitution Test (LDST), the Digit Symbol Substitution Task (DSST), semantic and phonemic fluency tests, and the Stroop Color and Word Test. Replication was sought in 1311-21860 subjects from 20 independent cohorts. A significant association was observed in the discovery cohorts for the single-nucleotide polymorphism (SNP) rs17518584 (discovery P-value=3.12 × 10(-8)) and in the joint discovery and replication meta-analysis (P-value=3.28 × 10(-9) after adjustment for age, gender and education) in an intron of the gene cell adhesion molecule 2 (CADM2) for performance on the LDST/DSST. Rs17518584 is located about 170 kb upstream of the transcription start site of the major transcript for the CADM2 gene, but is within an intron of a variant transcript that includes an alternative first exon. The variant is associated with expression of CADM2 in the cingulate cortex (P-value=4 × 10(-4)). The protein encoded by CADM2 is involved in glutamate signaling (P-value=7.22 × 10(-15)), gamma-aminobutyric acid (GABA) transport (P-value=1.36 × 10(-11)) and neuron cell-cell adhesion (P-value=1.48 × 10(-13)). Our findings suggest that genetic variation in the CADM2 gene is associated with individual differences in information processing speed.

126 citations

Carla A. Ibrahim-Verbaas, Jan Bressler, Stéphanie Debette, Maaike Schuur, Albert V. Smith, J. C. Bis, G. Davies, S. Trompet, Jennifer A. Smith, Christiane Wolf, Lori B. Chibnik, Yongmei Liu, Veronique Vitart, Mirna Kirin, K. Petrovic, Ozren Polasek, Lina Zgaga, Chloe Fawns-Ritchie, Peter Hoffmann, Juha Karjalainen, Jari Lahti, David J. Llewellyn, Christian Schmidt, Karen A. Mather, Vincent Chouraki, Qi Sun, Susan M. Resnick, Ludger Rose, Christopher Oldmeadow, Marlene C. W. Stewart, Blair H. Smith, Vilmundur Gudnason, Qiong Yang, Saira Saeed Mirza, Joop Jukema, Philip L. DeJager, T.B. Harris, D C Liewald, Najaf Amin, Laura H. Coker, Oliver Stegle, Oscar L. Lopez, R. Schmidt, A. Teumer, Ian Ford, Nazanin Karbalai, James T. Becker, Maria K. Jonsdottir, Rhoda Au, Rudolf S N Fehrmann, Stefan Herms, Michael A. Nalls, Wei Zhao, Stephen T. Turner, Kristine Yaffe, Kurt Lohman, J. C. van Swieten, Sharon L.R. Kardia, D. S. Knopman, William M. Meeks, Gerardo Heiss, Elizabeth G. Holliday, Peter W. Schofield, Toshiko Tanaka, David J. Stott, Jing Wang, Paul M. Ridker, Alan J. Gow, Alison Pattie, John M. Starr, Lynne J. Hocking, Nicola J. Armstrong, Stela McLachlan, Joshua M. Shulman, Luke C. Pilling, G. Eiriksdottir, Rodney J. Scott, Nicole A. Kochan, Aarno Palotie, Y-C Hsieh, Johan G. Eriksson, Alan D. Penman, Rebecca F. Gottesman, B.A. Oostra, Le Yu, Anita L. DeStefano, Alexa S. Beiser, Melissa Garcia, Jerome I. Rotter, Markus M. Noethen, Albert Hofman, P.E. Slagboom, R.G.J. Westendorp, Brendan M. Buckley, Philip A. Wolf, André G. Uitterlinden, Bruce M. Psaty, Hans-Jörgen Grabe, Stefania Bandinelli, Daniel I. Chasman, Francine Grodstein, K. Roikkonen, J-C Lambert, David J. Porteous, Jenna Price, Perminder S. Sachdev, L Ferrucci, John Attia, Igor Rudan, Caroline Hayward, Antony Wright, James F. Wilson, Sven Cichon, Lude Franke, H. Schmidt, Jun Ding, A.J.M. de Craen, Myriam Fornage, David A. Bennett, Ian J. Deary, M. A. Ikram, L. J. Launer, Annette L. Fitzpatrick, Sudha Seshadri, C M van Duijn, Thomas H. Mosley 
17 Mar 2016
TL;DR: A genome-wide association study of executive functioning and information processing speed in non-demented older adults from the CHARGE consortium suggests that genetic variation in the CADM2 gene is associated with individual differences in informationprocessing speed.
Abstract: To identify common variants contributing to normal variation in two specific domains of cognitive functioning, we conducted a genome-wide association study (GWAS) of executive functioning and information processing speed in non-demented older adults from the CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) consortium. Neuropsychological testing was available for 5429–32 070 subjects of European ancestry aged 45 years or older, free of dementia and clinical stroke at the time of cognitive testing from 20 cohorts in the discovery phase. We analyzed performance on the Trail Making Test parts A and B, the Letter Digit Substitution Test (LDST), the Digit Symbol Substitution Task (DSST), semantic and phonemic fluency tests, and the Stroop Color and Word Test. Replication was sought in 1311-21860 subjects from 20 independent cohorts. A significant association was observed in the discovery cohorts for the single-nucleotide polymorphism (SNP) rs17518584 (discovery P-value=3.12 × 10−8) and in the joint discovery and replication meta-analysis (P-value=3.28 × 10−9 after adjustment for age, gender and education) in an intron of the gene cell adhesion molecule 2 (CADM2) for performance on the LDST/DSST. Rs17518584 is located about 170 kb upstream of the transcription start site of the major transcript for the CADM2 gene, but is within an intron of a variant transcript that includes an alternative first exon. The variant is associated with expression of CADM2 in the cingulate cortex (P-value=4 × 10−4). The protein encoded by CADM2 is involved in glutamate signaling (P-value=7.22 × 10−15), gamma-aminobutyric acid (GABA) transport (P-value=1.36 × 10−11) and neuron cell-cell adhesion (P-value=1.48 × 10−13). Our findings suggest that genetic variation in the CADM2 gene is associated with individual differences in information processing speed.

113 citations

Journal ArticleDOI
Eveline Nüesch1, Eveline Nüesch2, Caroline Dale2, Tom Palmer3, Tom Palmer4, Jon White5, Brendan J. Keating6, E. P. A. van Iperen, Anuj Goel7, Sandosh Padmanabhan8, Folkert W. Asselbergs9, Folkert W. Asselbergs5, W.M.M. Verschuren, Cisca Wijmenga, Y. T. van der Schouw, N. C. Onland-Moret, Leslie A. Lange10, G K Hovingh, Suthesh Sivapalaratnam, Richard W Morris5, Peter H. Whincup11, G S Wannamethe5, Tom R. Gaunt12, Shah Ebrahim2, Laura Steel6, Nikhil Nair6, Alexander P. Reiner13, Charles Kooperberg13, James F. Wilson14, Jennifer L. Bolton14, Stela McLachlan14, Jenna Price14, Mark W. J. Strachan15, Christine Robertson14, Marcus E. Kleber16, Graciela E. Delgado16, Winfried März17, Olle Melander18, Anna F. Dominiczak8, Martin Farrall7, Hugh Watkins7, Maarten Leusink19, A.H. Maitland-van der Zee19, M C de Groot2, Frank Dudbridge2, Aroon D. Hingorani5, Yoav Ben-Shlomo12, Debbie A Lawlor12, Antoinette Amuzu, M Caufield, Alana Cavadino, John E. Cooper12, Teri-Louise Davies, Fotios Drenos12, Jorgen Engmann, Chris Finan, Claudia Giambartolomei, Rebecca Hardy12, Steve E. Humphries, Elina Hyppönen, Mika Kivimäki12, Diana Kuh, Meena Kumari, Ken K. Ong, Vincent Plagnol12, C Power, Marcus Richards, Svati H. Shah12, Tina Shah, Reecha Sofat, Philippa J. Talmud, N Wareham12, Helen R. Warren, John C. Whittaker12, Andrew Wong12, Delilah Zabaneh, G. Davey Smith6, G. Davey Smith5, G. Davey Smith20, Jonathan C. K. Wells21, David A. Leon22, David A. Leon2, Michael V. Holmes20, Michael V. Holmes6, Michael V. Holmes5, Juan P. Casas5, Juan P. Casas2 
TL;DR: Taller individuals have a lower risk of CHD with potential explanations being that taller people have a better lung function and lower levels of body mass index, cholesterol and blood pressure.
Abstract: Background: We investigated causal effect of completed growth, measured by adult height, on coronary heart disease (CHD), stroke and cardiovascular traits, using instrumental variable (IV) Mendelian randomization meta-analysis. Methods: We developed an allele score based on 69 single nucleotide polymorphisms (SNPs) associated with adult height, identified by the IBCCardioChip, and used it for IV analysis against cardiovascular risk factors and events in 21 studies and 60 028 participants. IV analysis on CHD was supplemented by summary data from 180 height-SNPs from the GIANT consortium and their corresponding CHD estimates derived from CARDIoGRAMplusC4D. Results: IV estimates from IBCCardioChip and GIANT-CARDIoGRAMplusC4D showed that a 6.5-cm increase in height reduced the odds of CHD by 10% [odds ratios 0.90; 95% confidence intervals (CIs): 0.78 to 1.03 and 0.85 to 0.95, respectively],which agrees with the estimate from the Emerging Risk Factors Collaboration (hazard ratio 0.93; 95% CI: 0.91 to 0.94). IV analysis revealed no association with stroke (odds ratio 0.97; 95% CI: 0.79 to 1.19). IV analysis showed that a 6.5-cm increase in height resulted in lower levels of body mass index (P < 0.001), triglycerides (P < 0.001), non high-density (non-HDL) cholesterol (P < 0.001), C-reactive protein (P = 0.042), and systolic blood pressure (P = 0.064) and higher levels of forced expiratory volume in 1 s and forced vital capacity (P < 0.001 for both). Conclusions: Taller individuals have a lower risk of CHD with potential explanations being that taller people have a better lung function and lower levels of body mass index, cholesterol and blood pressure.

108 citations

Journal ArticleDOI
Nora Franceschini1, Claudia Giambartolomei2, P. De Vries3, Chris Finan4  +167 moreInstitutions (62)
TL;DR: The authors identify and prioritize genetic loci for cIMT and plaque by GWAS and colocalization approaches and further demonstrate genetic correlation with CHD and stroke.
Abstract: Carotid artery intima media thickness (cIMT) and carotid plaque are measures of subclinical atherosclerosis associated with ischemic stroke and coronary heart disease (CHD). Here, we undertake meta-analyses of genome-wide association studies (GWAS) in 71,128 individuals for cIMT, and 48,434 individuals for carotid plaque traits. We identify eight novel susceptibility loci for cIMT, one independent association at the previously-identified PINX1 locus, and one novel locus for carotid plaque. Colocalization analysis with nearby vascular expression quantitative loci (cis-eQTLs) derived from arterial wall and metabolic tissues obtained from patients with CHD identifies candidate genes at two potentially additional loci, ADAMTS9 and LOXL4. LD score regression reveals significant genetic correlations between cIMT and plaque traits, and both cIMT and plaque with CHD, any stroke subtype and ischemic stroke. Our study provides insights into genes and tissue-specific regulatory mechanisms linking atherosclerosis both to its functional genomic origins and its clinical consequences in humans.

96 citations


Cited by
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TL;DR: Antiinflammatory therapy targeting the interleukin‐1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid‐level lowering.
Abstract: BackgroundExperimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. MethodsWe conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. ResultsAt 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in t...

5,660 citations

Journal ArticleDOI
TL;DR: This year's edition of the Statistical Update includes data on the monitoring and benefits of cardiovascular health in the population, metrics to assess and monitor healthy diets, an enhanced focus on social determinants of health, a focus on the global burden of cardiovascular disease, and further evidence-based approaches to changing behaviors, implementation strategies, and implications of the American Heart Association’s 2020 Impact Goals.
Abstract: Background: The American Heart Association, in conjunction with the National Institutes of Health, annually reports on the most up-to-date statistics related to heart disease, stroke, and cardiovas...

5,078 citations

01 Feb 2015
TL;DR: In this article, the authors describe the integrative analysis of 111 reference human epigenomes generated as part of the NIH Roadmap Epigenomics Consortium, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression.
Abstract: The reference human genome sequence set the stage for studies of genetic variation and its association with human disease, but epigenomic studies lack a similar reference. To address this need, the NIH Roadmap Epigenomics Consortium generated the largest collection so far of human epigenomes for primary cells and tissues. Here we describe the integrative analysis of 111 reference human epigenomes generated as part of the programme, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression. We establish global maps of regulatory elements, define regulatory modules of coordinated activity, and their likely activators and repressors. We show that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease. Our results demonstrate the central role of epigenomic information for understanding gene regulation, cellular differentiation and human disease.

4,409 citations

Journal ArticleDOI
TL;DR: The American Heart Association, in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascul...
Abstract: Background: The American Heart Association, in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascul...

3,034 citations

Journal ArticleDOI
TL;DR: It is concluded that Mendelian randomization investigations using summarized data from uncorrelated variants are similarly efficient to those using individual‐level data, although the necessary assumptions cannot be so fully assessed.
Abstract: Genome-wide association studies, which typically report regression coefficients summarizing the associations of many genetic variants with various traits, are potentially a powerful source of data for Mendelian randomization investigations. We demonstrate how such coefficients from multiple variants can be combined in a Mendelian randomization analysis to estimate the causal effect of a risk factor on an outcome. The bias and efficiency of estimates based on summarized data are compared to those based on individual-level data in simulation studies. We investigate the impact of gene–gene interactions, linkage disequilibrium, and ‘weak instruments’ on these estimates. Both an inverse-variance weighted average of variant-specific associations and a likelihood-based approach for summarized data give similar estimates and precision to the two-stage least squares method for individual-level data, even when there are gene–gene interactions. However, these summarized data methods overstate precision when variants are in linkage disequilibrium. If the P-value in a linear regression of the risk factor for each variant is less than , then weak instrument bias will be small. We use these methods to estimate the causal association of low-density lipoprotein cholesterol (LDL-C) on coronary artery disease using published data on five genetic variants. A 30% reduction in LDL-C is estimated to reduce coronary artery disease risk by 67% (95% CI: 54% to 76%). We conclude that Mendelian randomization investigations using summarized data from uncorrelated variants are similarly efficient to those using individual-level data, although the necessary assumptions cannot be so fully assessed.

2,003 citations