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Your search keyword '"Nelson, B."' showing total 6 results
6 results on '"Nelson, B."'

1. Contribution of copy number variants to schizophrenia from a genome-wide study of 41,321 subjects

Author

Patricia T. Michie, Franziska Degenhardt, Brandon Wormley, Paola Giusti-Rodríguez, Mark J. Daly, Raquelle I. Mesholam-Gately, Ingrid Melle, Sibylle G. Schwab, Andrew McQuillin, Benjamin M. Neale, Joshua L. Roffman, Abraham Reichenberg, Pamela Sklar, Diana O. Perkins, Jennifer L. Moran, Donald W. Black, Per Hoffmann, A. Hofman, Hailiang Huang, John L. Waddington, Giulio Genovese, Aaron R. Wolen, Deborah L. Levy, David Curtis, Digby Quested, Carlos N. Pato, Nicholas John Craddock, Stephanie Williams, Kung Yee Liang, Zhouzhi Wang, Tracey L. Petryshen, Ann E. Pulver, Randy L. Buckner, Stephan Ripke, Roel A. Ophoff, Danielle Posthuma, Lili Milani, Jacques Mallet, Menachem Fromer, Christian R. Marshall, Jaana Suvisaari, Jana Strohmaier, Richard Bruggeman, Marcella Rietschel, Ayman H. Fanous, Andrew M. McIntosh, James T.R. Walters, Dimitris Dikeos, Panos Roussos, Veikko Salomaa, Aiden Corvin, Carin J. Meijer, Tiina Paunio, Assen Jablensky, Sarah E. Bergen, Nancy G. Buccola, Annelie Nordin, Wolfgang Maier, Srdjan Djurovic, Naomi R. Wray, Aniket Shetty, Joel Eriksson, Dan Rujescu, Jouko Lönnqvist, Brian Kelly, Wenting Wu, Alexander Richards, Frans Henskens, Rich Belliveau, Bryan J. Mowry, Elodie Drapeau, Andreas J. Forstner, Silviu Alin Bacanu, Jubao Duan, Tõnu Esko, Bernard Lerer, Carmel M. Loughland, Olli Pietiläinen, Michael Conlon O'Donovan, Shaun M. Purcell, Michael Gill, Thomas G. Schulze, Douglas S. Greer, Stephen W. Scherer, Eli A. Stahl, Markus M. Nöthen, Guiqing Cai, William M. Brandler, Kristin K. Nicodemus, Dominique Campion, David A. Collier, Farooq Amin, Joel N. Hirschhorn, Robin M. Murray, Timothy G. Dinan, Mark Reimers, Murray J. Cairns, Rodney J. Scott, Aarno Palotie, Robert Freedman, Nelson B. Freimer, Joshua R. Atkins, Gary Donohoe, Ann Olincy, Jonathan Sebat, Colm McDonald, Srinivas Thirumalai, John Powell, Jo Knight, Vahram Haroutunian, Dieter B. Wildenauer, Tim B. Bigdeli, Lieuwe de Haan, Peter Eichhammer, James J. Crowley, Lynn E. DeLisi, Ulrich Schall, Rolf Adolfsson, Marcelo Bertalan, Thomas Hansen, Eric Strengman, Michael Davidson, Dheeraj Malhotra, Manuel Mattheisen, Jeffrey A. Lieberman, Benedicto Crespo-Facorro, Stephanie Godard, Edward M. Scolnick, Jonathan Pimm, Bertram Müller-Myhsok, Qingqin Li, Michele T. Pato, Wiepke Cahn, Christos Pantelis, Ingrid Agartz, Brendan Bulik-Sullivan, Madhusudan Gujral, Martilias S. Farrell, Brady J. Maher, Laurent Essioux, Karin V Fuentes Fajarado, Andres Metspalu, Stephanie H. Witt, Patrick F. Sullivan, Mark Weiser, Younes Mokrab, Kai How Farh, Line Olsen, Dermot Walsh, Peter Holmans, Hugh Gurling, Joseph I. Friedman, Andrew Pocklington, Daniel P. Howrigan, Lude Franke, Tune H. Pers, Larry J. Seidman, Pablo V. Gejman, Dalila Pinto, Michael John Owen, Inez Myin-Germeys, Steven A. McCarroll, Wei Cheng, Jackie Goldstein, C. Robert Cloninger, Elliot S. Gershon, Deborah A. Nertney, Thomas Werge, Noa Carrera, Kieran C. Murphy, Rita M. Cantor, Ariel Darvasi, Mark Hansen, Annette M. Hartmann, Ole A. Andreassen, Bradley T. Webb, Henrik B. Rasmussen, David Cohen, Elvira Bramon, Erik G. Jönsson, Vaughan J. Carr, Pui Y. Lee, Masashi Ikeda, Daniele Merico, Danny Antaki, Brien P. Riley, Stefan Herms, Igor Nenadic, Bettina Konte, Kimberley D. Chambert, Jurgen Del Favero, George Kirov, Matthew C. Keller, Jacob Gratten, Douglas F. Levinson, Luba Kalaydjieva, Bhooma Thiruvahindrapuram, Alan R. Sanders, Sang-Yun Oh, Alkes L. Price, Vihra Milanova, Juha Veijola, Erik Söderman, Dragan M. Svrakic, David H. Kavanagh, Patrik K. E. Magnusson, Douglas Blackwood, Nakao Iwata, Jim van Os, Jeremy M. Silverman, Elena Parkhomenko, Kenneth L. Davis, Jing Qin Wu, Eadbhard O'Callaghan, Chris C. A. Spencer, Juha Karjalainen, Anna K. Kähler, Clement C. Zai, Nigel Williams, Joseph D. Buxbaum, Jin P. Szatkiewicz, Laura Nisenbaum, Sang Hong Lee, Yunjung Kim, Colm O'Dushlaine, René S. Kahn, Morten Mattingsdal, Inge Joa, Marian L. Hamshere, Frank Dudbridge, Ina Giegling, Sandra Meier, Derek W. Morris, Robert W. McCarley, Douglas M. Ruderfer, Paul Cormican, Lyudmila Georgieva, Sven Cichon, Josef Frank, Jianxin Shi, George N. Papadimitriou, Kenneth S. Kendler, Margot Albus, Enrico Domenici, Claudine Laurent, Francis A. O'Neill, Adam Savitz, Jordan W. Smoller, James L. Kennedy, Peter M. Visscher, Valentina Escott-Price, Christina M. Hultman, T. Scott Stroup, Elizabeth Bevilacqua, James A. Knowles, William Byerley, Paul A. Tooney, Madeline Alexander, Stanley V. Catts, David St Clair, Sophie E. Legge, Gerald Nestadt, Michelle S. Maile, Perceptual and Cognitive Neuroscience (PCN), Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Clinical Cognitive Neuropsychiatry Research Program (CCNP), Stem Cell Aging Leukemia and Lymphoma (SALL), Psychiatrie & Neuropsychologie, RS: MHeNs - R2 - Mental Health, MUMC+: Hersen en Zenuw Centrum (3), MUMC+: MA Psychiatrie (3), Complex Trait Genetics, Amsterdam Neuroscience - Complex Trait Genetics, APH - Mental Health, ANS - Complex Trait Genetics, Adult Psychiatry, Other departments, Marshall, Christian R, Howrigan, Daniel P, Merico, Daniele, Thiruvahindrapuram, Bhooma, Lee, S Hong, Sebat, Jonathan, Psychosis Endophenotypes International Consortium, CNV and Schizophrenia Working Groups of the Psychiatric Genomics Consortium, CNV, Schizophrenia Working Grp, Psychosis Endophenotypes, Rehabilitation Medicine, and Child and Adolescent Psychiatry / Psychology

Subjects
0301 basic medicine, Male, 16P11.2, Duplication, Autism, Rearrangement, Genome-wide association study, Copy number variant, Gene, Medical and Health Sciences, 0302 clinical medicine, DUPLICATIONS, Risk Factors, Gene duplication, Genotype, Disorder, Copy-number variation, Genetics, Genetics & Heredity, RISK, copy number variation, REARRANGEMENTS, Biological Sciences, 16p11.2, 3. Good health, Phenotype, Female, Risk, CNVS, Genetic Markers, genetic etiology, CNV and Schizophrenia Working Groups of the Psychiatric Genomics Consortium, DNA Copy Number Variations, DISORDERS, CNV, Non-allelic homologous recombination, PHENOTYPES, Biology, 03 medical and health sciences, SDG 3 - Good Health and Well-being, genomics, Journal Article, Humans, Comparative Study, Genetic Predisposition to Disease, AUTISM, Psychosis Endophenotypes International Consortium, MUTATIONS, Case-control study, Odds ratio, R1, GENE, 030104 developmental biology, genetics research, Genetic marker, Genetic Loci, Case-Control Studies, Mutation, Schizophrenia, Human medicine, 030217 neurology & neurosurgery, Developmental Biology, Genome-Wide Association Study
Abstract

Copy number variants (CNVs) have been strongly implicated in the genetic etiology of schizophrenia (SCZ). However, genome-wide investigation of the contribution of CNV to risk has been hampered by limited sample sizes. We sought to address this obstacle by applying a centralized analysis pipeline to a SCZ cohort of 21,094 cases and 20,227 controls. A global enrichment of CNV burden was observed in cases (odds ratio (OR) = 1.11, P = 5.7 x 10(-15)), which persisted after excluding loci implicated in previous studies (OR = 1.07, P = 1.7 x 10(-6)). CNV burden was enriched for genes associated with synaptic function (OR = 1.68, P = 2.8 x 10(-11)) and neurobehavioral phenotypes in mouse (OR = 1.18, P = 7.3 x 10(-5)). Genome-wide significant evidence was obtained for eight loci, including 1q21.1, 2p16.3 (NRXN1), 3q29, 7q11.2, 15q13.3, distal 16p11.2, proximal 16p11.2 and 22q11.2. Suggestive support was found for eight additional candidate susceptibility and protective loci, which consisted predominantly of CNVs mediated by nonallelic homologous recombination. Refereed/Peer-reviewed

Published
2017

2. Extensions of Multiple-Group Item Response Theory Alignment: Application to Psychiatric Phenotypes in an International Genomics Consortium.

Author

Mansolf, Maxwell, Vreeker, Annabel, Reise, Steven P., Freimer, Nelson B., Glahn, David C., Gur, Raquel E., Moore, Tyler M., Pato, Carlos N., Pato, Michele T., Palotie, Aarno, Holm, Minna, Suvisaari, Jaana, Partonen, Timo, Kieseppä, Tuula, Paunio, Tiina, Boks, Marco, Kahn, René, Ophoff, Roel A., Bearden, Carrie E., and Loohuis, Loes Olde

Subjects
GENOMES, MENTAL illness, RESEARCH funding, PHENOTYPES, GENOMICS, STATISTICAL models, SEQUENCE analysis, DIFFERENTIAL item functioning (Research bias)
Abstract

Large-scale studies spanning diverse project sites, populations, languages, and measurements are increasingly important to relate psychological to biological variables. National and international consortia already are collecting and executing mega-analyses on aggregated data from individuals, with different measures on each person. In this research, we show that Asparouhov and Muthén's alignment method can be adapted to align data from disparate item sets and response formats. We argue that with these adaptations, the alignment method is well suited for combining data across multiple sites even when they use different measurement instruments. The approach is illustrated using data from the Whole Genome Sequencing in Psychiatric Disorders consortium and a real-data-based simulation is used to verify accurate parameter recovery. Factor alignment appears to increase precision of measurement and validity of scores with respect to external criteria. The resulting parameter estimates may further inform development of more effective and efficient methods to assess the same constructs in prospectively designed studies. [ABSTRACT FROM AUTHOR]

Published
2020
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3. Characterization of Expression Quantitative Trait Loci in Pedigrees from Colombia and Costa Rica Ascertained for Bipolar Disorder

Author

Christine B. Peterson, Susan K. Service, Anna J. Jasinska, Fuying Gao, Ivette Zelaya, Terri M. Teshiba, Carrie E. Bearden, Rita M. Cantor, Victor I. Reus, Gabriel Macaya, Carlos López-Jaramillo, Marina Bogomolov, Yoav Benjamini, Eleazar Eskin, Giovanni Coppola, Nelson B. Freimer, Chiara Sabatti, and Brown, Christopher David

Subjects
Male, 0301 basic medicine, Cancer Research, Heredity, Bipolar Disorder, Gene Expression, Genome-wide association study, QH426-470, 0302 clinical medicine, Missing heritability problem, Medicine and Health Sciences, 2.1 Biological and endogenous factors, Gene Regulatory Networks, Aetiology, Genetics (clinical), Genetics, education.field_of_study, Chromosome Mapping, Genomics, Single Nucleotide, Phenotypes, Female, Research Article, Biotechnology, Costa Rica, DNA transcription, Quantitative Trait Loci, Population, Locus (genetics), Colombia, Quantitative trait locus, Biology, Expression QuantitativeTrait Loci, Polymorphism, Single Nucleotide, 03 medical and health sciences, Gene mapping, Mental Health and Psychiatry, Humans, Gene Regulation, Genetic Predisposition to Disease, Genetic Testing, Polymorphism, Gene Prediction, education, Molecular Biology, Alleles, Ecology, Evolution, Behavior and Systematics, Evolutionary Biology, Population Biology, Mood Disorders, Human Genome, Biology and Life Sciences, Computational Biology, Heritability, Genome Analysis, 030104 developmental biology, Expression quantitative trait loci, Population Genetics, 030217 neurology & neurosurgery, Genome-Wide Association Study, Developmental Biology
Abstract

The observation that variants regulating gene expression (expression quantitative trait loci, eQTL) are at a high frequency among SNPs associated with complex traits has made the genome-wide characterization of gene expression an important tool in genetic mapping studies of such traits. As part of a study to identify genetic loci contributing to bipolar disorder and other quantitative traits in members of 26 pedigrees from Costa Rica and Colombia, we measured gene expression in lymphoblastoid cell lines derived from 786 pedigree members. The study design enabled us to comprehensively reconstruct the genetic regulatory network in these families, provide estimates of heritability, identify eQTL, evaluate missing heritability for the eQTL, and quantify the number of different alleles contributing to any given locus. In the eQTL analysis, we utilize a recently proposed hierarchical multiple testing strategy which controls error rates regarding the discovery of functional variants. Our results elucidate the heritability and regulation of gene expression in this unique Latin American study population and identify a set of regulatory SNPs which may be relevant in future investigations of complex disease in this population. Since our subjects belong to extended families, we are able to compare traditional kinship-based estimates with those from more recent methods that depend only on genotype information., Author Summary We assess the heritability and genetic regulation of gene expression in a population of 786 individuals from Costa Rica and Colombia. The subjects, originally recruited in a study of bipolar disorder, are related within 26 extended families. This design allows us to compare estimates of the heritability of gene expression obtained using both traditional and genotype-based methods. We address questions regarding the architecture of genetic regulation including the extent to which gene expression is influenced by variants located nearby vs. far away on the genome and how many variants affect the expression of a given gene. In addition, we identify genetic variants which regulate gene expression; these serve as candidates for future studies to establish the genetic basis of complex traits, including those related to bipolar disorder, and also provide insight into the architecture of genetic regulation in this unique Latin American study population.

Published
2016

4. Distribution and Medical Impact of Loss-of-Function Variants in the Finnish Founder Population

Author

Domenico Girelli, Svati H. Shah, Seppo Koskinen, Mark I. McCarthy, Reedik Mägi, Yingleong Chan, Joel N. Hirschhorn, Aarno Palotie, Muredach P. Reilly, G K Hovingh, Hugh Watkins, Taru Tukiainen, Claes Ladenvall, Jason Flannick, Eija Hämäläinen, Suzannah Bumpstead, Markus Perola, Mark J. Daly, Leif Groop, Diego Ardissino, Aki S. Havulinna, Stacey Gabriel, Veikko Salomaa, Priit Palta, Michael Boehnke, Xueling Sim, Jeffrey C. Barrett, Rany M. Salem, Peter Würtz, Alexander P. Reiner, Ruth McPherson, Tõnu Esko, Monkol Lek, Andres Metspalu, Sekar Kathiresan, Karola Rehnström, Cecilia M. Lindgren, Sirpa Jalkanen, Stefan Blankenberg, Nathan O. Stitziel, Benjamin D. Horne, Nelson B. Freimer, Anuj Goel, Mikael Maksimow, Michael Inouye, Daniel G. MacArthur, Olli T. Raitakari, Richard Durbin, Martin Farrall, Terho Lehtimäki, Kristiina Aalto, Tanja Zeller, Tuuli Lappalainen, David Altshuler, Markku Laakso, Samuli Ripatti, Marko Salmi, Elaine T. Lim, Alisa K. Manning, Jaakko Kaprio, Institute for Molecular Medicine Finland, University of Helsinki, Hjelt Institute (-2014), Department of Public Health, Quantitative Genetics, Biostatistics Helsinki, Complex Disease Genetics, Genomics of Neurological and Neuropsychiatric Disorders, Genetic Epidemiology, Cutler, David, Massachusetts Institute of Technology. Department of Biology, Altshuler, David, Inouye, Michael [0000-0001-9413-6520], Durbin, Richard [0000-0002-9130-1006], Apollo - University of Cambridge Repository, ACS - Amsterdam Cardiovascular Sciences, and Vascular Medicine

Subjects
Male, Cancer Research, Heredity, Genome-wide association study, Cardiovascular, whole exome sequencing, Gene Frequency, 2.1 Biological and endogenous factors, Exome, Aetiology, Finland, Genetics (clinical), Exome sequencing, Genetics, education.field_of_study, low-frequency loss-of-function variants, Cardiovascular disease, Genomics, Sequencing Initiative Suomi (SISu) Project, Founder Effect, 3. Good health, Phenotypes, Phenotype, Genetic Diseases, Female, Allelic heterogeneity, Research Article, Common disease-common variant, lcsh:QH426-470, Population, European Continental Ancestry Group, education, Biology, ta3111, White People, Genetic Disorders, Mendelian randomization, Genome-Wide Association Studies, Gene Disruption, Humans, Molecular Biology, Genetic Association Studies, Ecology, Evolution, Behavior and Systematics, Evolutionary Biology, Quantitative Traits, Whites, Genetic Drift, Human Genome, Genetic Diseases, Inborn, Biology and Life Sciences, Computational Biology, Genetic Variation, Human Genetics, Genome Analysis, lcsh:Genetics, Genetics, Population, Inborn, Genetics of Disease, Generic health relevance, 3111 Biomedicine, Population Genetics, Genome-Wide Association Study, Developmental Biology, Founder effect
Abstract

Exome sequencing studies in complex diseases are challenged by the allelic heterogeneity, large number and modest effect sizes of associated variants on disease risk and the presence of large numbers of neutral variants, even in phenotypically relevant genes. Isolated populations with recent bottlenecks offer advantages for studying rare variants in complex diseases as they have deleterious variants that are present at higher frequencies as well as a substantial reduction in rare neutral variation. To explore the potential of the Finnish founder population for studying low-frequency (0.5–5%) variants in complex diseases, we compared exome sequence data on 3,000 Finns to the same number of non-Finnish Europeans and discovered that, despite having fewer variable sites overall, the average Finn has more low-frequency loss-of-function variants and complete gene knockouts. We then used several well-characterized Finnish population cohorts to study the phenotypic effects of 83 enriched loss-of-function variants across 60 phenotypes in 36,262 Finns. Using a deep set of quantitative traits collected on these cohorts, we show 5 associations (p, National Institutes of Health (U.S.) (NIH RC2 HL-102925)

Published
2014

5. Characterization of Expression Quantitative Trait Loci in Pedigrees from Colombia and Costa Rica Ascertained for Bipolar Disorder.

Author

Peterson, Christine B., Service, Susan K., Jasinska, Anna J., Gao, Fuying, Zelaya, Ivette, Teshiba, Terri M., Bearden, Carrie E., Cantor, Rita M., Reus, Victor I., Macaya, Gabriel, López-Jaramillo, Carlos, Bogomolov, Marina, Benjamini, Yoav, Eskin, Eleazar, Coppola, Giovanni, Freimer, Nelson B., and Sabatti, Chiara

Subjects
GENETICS of bipolar disorder, LYMPHOBLASTOID cell lines, GENE expression, HERALDRY, BIPOLAR disorder in adolescence
Abstract

The observation that variants regulating gene expression (expression quantitative trait loci, eQTL) are at a high frequency among SNPs associated with complex traits has made the genome-wide characterization of gene expression an important tool in genetic mapping studies of such traits. As part of a study to identify genetic loci contributing to bipolar disorder and other quantitative traits in members of 26 pedigrees from Costa Rica and Colombia, we measured gene expression in lymphoblastoid cell lines derived from 786 pedigree members. The study design enabled us to comprehensively reconstruct the genetic regulatory network in these families, provide estimates of heritability, identify eQTL, evaluate missing heritability for the eQTL, and quantify the number of different alleles contributing to any given locus. In the eQTL analysis, we utilize a recently proposed hierarchical multiple testing strategy which controls error rates regarding the discovery of functional variants. Our results elucidate the heritability and regulation of gene expression in this unique Latin American study population and identify a set of regulatory SNPs which may be relevant in future investigations of complex disease in this population. Since our subjects belong to extended families, we are able to compare traditional kinship-based estimates with those from more recent methods that depend only on genotype information. [ABSTRACT FROM AUTHOR]

Published
2016
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6. Distribution and Medical Impact of Loss-of-Function Variants in the Finnish Founder Population

Author

Lim, Elaine T., Würtz, Peter, Havulinna, Aki S., Palta, Priit, Tukiainen, Taru, Rehnström, Karola, Esko, Tõnu, Mägi, Reedik, Inouye, Michael, Lappalainen, Tuuli, Chan, Yingleong, Salem, Rany M., Lek, Monkol, Flannick, Jason, Sim, Xueling, Manning, Alisa, Ladenvall, Claes, Bumpstead, Suzannah, Hämäläinen, Eija, Aalto, Kristiina, Maksimow, Mikael, Salmi, Marko, Blankenberg, Stefan, Ardissino, Diego, Shah, Svati, Horne, Benjamin, McPherson, Ruth, Hovingh, Gerald K., Reilly, Muredach P., Watkins, Hugh, Goel, Anuj, Farrall, Martin, Girelli, Domenico, Reiner, Alex P., Stitziel, Nathan O., Kathiresan, Sekar, Gabriel, Stacey, Barrett, Jeffrey C., Lehtimäki, Terho, Laakso, Markku, Groop, Leif, Kaprio, Jaakko, Perola, Markus, McCarthy, Mark I., Boehnke, Michael, Altshuler, David M., Lindgren, Cecilia M., Hirschhorn, Joel N., Metspalu, Andres, Freimer, Nelson B., Zeller, Tanja, Jalkanen, Sirpa, Koskinen, Seppo, Raitakari, Olli, Durbin, Richard, MacArthur, Daniel G., Salomaa, Veikko, Ripatti, Samuli, Daly, Mark J., and Palotie, Aarno

Subjects
Biology and Life Sciences, Computational Biology, Genome Analysis, Genome-Wide Association Studies, Evolutionary Biology, Population Genetics, Genetics, Genetics of Disease, Genetic Disorders, Heredity, Quantitative Traits, Human Genetics, Genetic Association Studies, Gene Disruption, Genomics, Phenotypes
Abstract

Exome sequencing studies in complex diseases are challenged by the allelic heterogeneity, large number and modest effect sizes of associated variants on disease risk and the presence of large numbers of neutral variants, even in phenotypically relevant genes. Isolated populations with recent bottlenecks offer advantages for studying rare variants in complex diseases as they have deleterious variants that are present at higher frequencies as well as a substantial reduction in rare neutral variation. To explore the potential of the Finnish founder population for studying low-frequency (0.5–5%) variants in complex diseases, we compared exome sequence data on 3,000 Finns to the same number of non-Finnish Europeans and discovered that, despite having fewer variable sites overall, the average Finn has more low-frequency loss-of-function variants and complete gene knockouts. We then used several well-characterized Finnish population cohorts to study the phenotypic effects of 83 enriched loss-of-function variants across 60 phenotypes in 36,262 Finns. Using a deep set of quantitative traits collected on these cohorts, we show 5 associations (p<5×10−8) including splice variants in LPA that lowered plasma lipoprotein(a) levels (P = 1.5×10−117). Through accessing the national medical records of these participants, we evaluate the LPA finding via Mendelian randomization and confirm that these splice variants confer protection from cardiovascular disease (OR = 0.84, P = 3×10−4), demonstrating for the first time the correlation between very low levels of LPA in humans with potential therapeutic implications for cardiovascular diseases. More generally, this study articulates substantial advantages for studying the role of rare variation in complex phenotypes in founder populations like the Finns and by combining a unique population genetic history with data from large population cohorts and centralized research access to National Health Registers.

Published
2014
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