Institution
University of Iceland
Education•Reykjavik, Suðurnes, Iceland•
About: University of Iceland is a education organization based out in Reykjavik, Suðurnes, Iceland. It is known for research contribution in the topics: Population & Genome-wide association study. The organization has 5423 authors who have published 16199 publications receiving 694762 citations. The organization is also known as: Háskóli Íslands.
Papers published on a yearly basis
Papers
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VU University Amsterdam1, Karolinska Institutet2, deCODE genetics3, Vanderbilt University4, Jönköping University5, University of Oslo6, Oslo University Hospital7, King's College London8, Stavanger University Hospital9, Akershus University Hospital10, University of Tromsø11, Innlandet Hospital Trust12, Norwegian University of Science and Technology13, University of California, San Francisco14, Vanderbilt University Medical Center15, University of Iceland16, University of Cambridge17, University of Bergen18, University College London19, Namsos Hospital20, University of North Carolina at Chapel Hill21, Broad Institute22, Charité23, Harvard University24, VU University Medical Center25
TL;DR: A large genome-wide association study of clinically diagnosed AD and AD-by-proxy identifies new loci and functional pathways that contribute to AD risk and adds novel insights into the neurobiology of AD.
Abstract: Alzheimer's disease (AD) is highly heritable and recent studies have identified over 20 disease-associated genomic loci. Yet these only explain a small proportion of the genetic variance, indicating that undiscovered loci remain. Here, we performed a large genome-wide association study of clinically diagnosed AD and AD-by-proxy (71,880 cases, 383,378 controls). AD-by-proxy, based on parental diagnoses, showed strong genetic correlation with AD (rg = 0.81). Meta-analysis identified 29 risk loci, implicating 215 potential causative genes. Associated genes are strongly expressed in immune-related tissues and cell types (spleen, liver, and microglia). Gene-set analyses indicate biological mechanisms involved in lipid-related processes and degradation of amyloid precursor proteins. We show strong genetic correlations with multiple health-related outcomes, and Mendelian randomization results suggest a protective effect of cognitive ability on AD risk. These results are a step forward in identifying the genetic factors that contribute to AD risk and add novel insights into the neurobiology of AD.
1,460 citations
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TL;DR: A common variant in the nicotinic acetylcholine receptor gene cluster on chromosome 15q24 with an effect on smoking quantity, ND and the risk of two smoking-related diseases in populations of European descent is identified.
Abstract: Smoking is a leading cause of preventable death, causing about 5 million premature deaths worldwide each year. Evidence for genetic influence on smoking behaviour and nicotine dependence (ND) has prompted a search for susceptibility genes. Furthermore, assessing the impact of sequence variants on smoking-related diseases is important to public health. Smoking is the major risk factor for lung cancer (LC) and is one of the main risk factors for peripheral arterial disease (PAD). Here we identify a common variant in the nicotinic acetylcholine receptor gene cluster on chromosome 15q24 with an effect on smoking quantity, ND and the risk of two smoking-related diseases in populations of European descent. The variant has an effect on the number of cigarettes smoked per day in our sample of smokers. The same variant was associated with ND in a previous genome-wide association study that used low-quantity smokers as controls, and with a similar approach we observe a highly significant association with ND. A comparison of cases of LC and PAD with population controls each showed that the variant confers risk of LC and PAD. The findings provide a case study of a gene-environment interaction, highlighting the role of nicotine addiction in the pathology of other serious diseases.
1,459 citations
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TL;DR: The causal network structure is a useful predictor of response to gene perturbations and presents a framework to test models of disease mechanisms underlying LOAD.
1,455 citations
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Aarhus University1, Lundbeck2, Harvard University3, Broad Institute4, Karolinska Institutet5, Cardiff University6, Statens Serum Institut7, QIMR Berghofer Medical Research Institute8, deCODE genetics9, University of Iceland10, Mental Health Services11, Charité12, University of California, Los Angeles13, Semel Institute for Neuroscience and Human Behavior14, University of Queensland15, Oslo University Hospital16, King's College London17, University of Toronto18, VU University Amsterdam19, Radboud University Nijmegen20, Veterans Health Administration21, Yale University22, Children's Hospital of Philadelphia23, Haukeland University Hospital24, University of Bergen25, University of Pennsylvania26, I.M. Sechenov First Moscow State Medical University27, Maastricht University28, University of Würzburg29, Goethe University Frankfurt30, Universidade Federal do Rio Grande do Sul31, Icahn School of Medicine at Mount Sinai32, University of North Carolina at Chapel Hill33, Emory University34, University of Copenhagen35, Aarhus University Hospital36, State University of New York Upstate Medical University37
TL;DR: A genome-wide association meta-analysis of 20,183 individuals diagnosed with ADHD and 35,191 controls identifies variants surpassing genome- wide significance in 12 independent loci and implicates neurodevelopmental pathways and conserved regions of the genome as being involved in underlying ADHD biology.
Abstract: Attention deficit/hyperactivity disorder (ADHD) is a highly heritable childhood behavioral disorder affecting 5% of children and 2.5% of adults. Common genetic variants contribute substantially to ADHD susceptibility, but no variants have been robustly associated with ADHD. We report a genome-wide association meta-analysis of 20,183 individuals diagnosed with ADHD and 35,191 controls that identifies variants surpassing genome-wide significance in 12 independent loci, finding important new information about the underlying biology of ADHD. Associations are enriched in evolutionarily constrained genomic regions and loss-of-function intolerant genes and around brain-expressed regulatory marks. Analyses of three replication studies: a cohort of individuals diagnosed with ADHD, a self-reported ADHD sample and a meta-analysis of quantitative measures of ADHD symptoms in the population, support these findings while highlighting study-specific differences on genetic overlap with educational attainment. Strong concordance with GWAS of quantitative population measures of ADHD symptoms supports that clinical diagnosis of ADHD is an extreme expression of continuous heritable traits.
1,436 citations
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Bjerknes Centre for Climate Research1, Stockholm University2, Saint Petersburg State University3, Russian Academy of Sciences4, University of Cambridge5, Geological Museum6, Gas Technology Institute7, Lund University8, University of Copenhagen9, Alfred Wegener Institute for Polar and Marine Research10, University of Iceland11, University of New Hampshire12, Geological Survey of Sweden13, University of Oulu14, Aarhus University15, Ohio State University16, Geological Survey of Finland17, University of Bristol18, Leibniz Association19
TL;DR: In this paper, the maximum limits of the Eurasian ice sheets during four glaciations have been reconstructed: (1) the Late Saalian (>140 ka), (2) the Early Weichselian (100-80 ka),(3) the Middle Weichsellian (60-50 ka), and (4) the late Weichselsian (25-15 ka) based on satellite data and aerial photographs combined with geological field investigations in Russia and Siberia, and with marine seismic and sediment core data.
1,426 citations
Authors
Showing all 5561 results
Name | H-index | Papers | Citations |
---|---|---|---|
Albert Hofman | 267 | 2530 | 321405 |
Kari Stefansson | 206 | 794 | 174819 |
Ronald Klein | 194 | 1305 | 149140 |
Eric Boerwinkle | 183 | 1321 | 170971 |
Unnur Thorsteinsdottir | 167 | 444 | 121009 |
Vilmundur Gudnason | 159 | 837 | 123802 |
Hakon Hakonarson | 152 | 968 | 101604 |
Bernhard O. Palsson | 147 | 831 | 85051 |
Andrew T. Hattersley | 146 | 768 | 106949 |
Fernando Rivadeneira | 146 | 628 | 86582 |
Rattan Lal | 140 | 1383 | 87691 |
Jonathan G. Seidman | 137 | 563 | 89782 |
Christine E. Seidman | 134 | 519 | 67895 |
Augustine Kong | 134 | 237 | 89818 |
Timothy M. Frayling | 133 | 500 | 100344 |