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Philip Asherson

Bio: Philip Asherson is an academic researcher from King's College London. The author has contributed to research in topics: Attention deficit hyperactivity disorder & Population. The author has an hindex of 91, co-authored 442 publications receiving 29480 citations. Previous affiliations of Philip Asherson include University of Cambridge & King's College.


Papers
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Journal ArticleDOI
S. Hong Lee1, Stephan Ripke2, Stephan Ripke3, Benjamin M. Neale3  +402 moreInstitutions (124)
TL;DR: Empirical evidence of shared genetic etiology for psychiatric disorders can inform nosology and encourages the investigation of common pathophysiologies for related disorders.
Abstract: Most psychiatric disorders are moderately to highly heritable. The degree to which genetic variation is unique to individual disorders or shared across disorders is unclear. To examine shared genetic etiology, we use genome-wide genotype data from the Psychiatric Genomics Consortium (PGC) for cases and controls in schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders (ASD) and attention-deficit/hyperactivity disorder (ADHD). We apply univariate and bivariate methods for the estimation of genetic variation within and covariation between disorders. SNPs explained 17-29% of the variance in liability. The genetic correlation calculated using common SNPs was high between schizophrenia and bipolar disorder (0.68 ± 0.04 s.e.), moderate between schizophrenia and major depressive disorder (0.43 ± 0.06 s.e.), bipolar disorder and major depressive disorder (0.47 ± 0.06 s.e.), and ADHD and major depressive disorder (0.32 ± 0.07 s.e.), low between schizophrenia and ASD (0.16 ± 0.06 s.e.) and non-significant for other pairs of disorders as well as between psychiatric disorders and the negative control of Crohn's disease. This empirical evidence of shared genetic etiology for psychiatric disorders can inform nosology and encourages the investigation of common pathophysiologies for related disorders.

2,058 citations

Journal ArticleDOI
Ditte Demontis1, Ditte Demontis2, Raymond K. Walters3, Raymond K. Walters4, Joanna Martin5, Joanna Martin6, Joanna Martin3, Manuel Mattheisen, Thomas Damm Als2, Thomas Damm Als1, Esben Agerbo1, Esben Agerbo2, Gisli Baldursson, Rich Belliveau3, Jonas Bybjerg-Grauholm7, Jonas Bybjerg-Grauholm2, Marie Bækvad-Hansen7, Marie Bækvad-Hansen2, Felecia Cerrato3, Kimberly Chambert3, Claire Churchhouse3, Claire Churchhouse4, Ashley Dumont3, Nicholas Eriksson, Michael J. Gandal, Jacqueline I. Goldstein4, Jacqueline I. Goldstein3, Katrina L. Grasby8, Jakob Grove, Olafur O Gudmundsson9, Olafur O Gudmundsson10, Christine Søholm Hansen2, Christine Søholm Hansen7, Christine Søholm Hansen11, Mads E. Hauberg2, Mads E. Hauberg1, Mads V. Hollegaard7, Mads V. Hollegaard2, Daniel P. Howrigan4, Daniel P. Howrigan3, Hailiang Huang4, Hailiang Huang3, Julian Maller3, Alicia R. Martin4, Alicia R. Martin3, Nicholas G. Martin8, Jennifer L. Moran3, Jonatan Pallesen2, Jonatan Pallesen1, Duncan S. Palmer4, Duncan S. Palmer3, Carsten Bøcker Pedersen1, Carsten Bøcker Pedersen2, Marianne Giørtz Pedersen1, Marianne Giørtz Pedersen2, Timothy Poterba4, Timothy Poterba3, Jesper Buchhave Poulsen2, Jesper Buchhave Poulsen7, Stephan Ripke3, Stephan Ripke4, Stephan Ripke12, Elise B. Robinson4, F. Kyle Satterstrom3, F. Kyle Satterstrom4, Hreinn Stefansson9, Christine Stevens3, Patrick Turley3, Patrick Turley4, G. Bragi Walters9, G. Bragi Walters10, Hyejung Won13, Hyejung Won14, Margaret J. Wright15, Ole A. Andreassen16, Philip Asherson17, Christie L. Burton18, Dorret I. Boomsma19, Bru Cormand, Søren Dalsgaard1, Barbara Franke20, Joel Gelernter21, Joel Gelernter22, Daniel H. Geschwind14, Daniel H. Geschwind13, Hakon Hakonarson23, Jan Haavik24, Jan Haavik25, Henry R. Kranzler21, Henry R. Kranzler26, Jonna Kuntsi17, Kate Langley6, Klaus-Peter Lesch27, Klaus-Peter Lesch28, Klaus-Peter Lesch29, Christel M. Middeldorp19, Christel M. Middeldorp15, Andreas Reif30, Luis Augusto Rohde31, Panos Roussos, Russell Schachar18, Pamela Sklar32, Edmund J.S. Sonuga-Barke17, Patrick F. Sullivan5, Patrick F. Sullivan33, Anita Thapar6, Joyce Y. Tung, Irwin D. Waldman34, Sarah E. Medland8, Kari Stefansson9, Kari Stefansson10, Merete Nordentoft35, Merete Nordentoft2, David M. Hougaard7, David M. Hougaard2, Thomas Werge2, Thomas Werge35, Thomas Werge11, Ole Mors2, Ole Mors36, Preben Bo Mortensen, Mark J. Daly, Stephen V. Faraone37, Anders D. Børglum1, Anders D. Børglum2, Benjamin M. Neale4, Benjamin M. Neale3 
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

Journal ArticleDOI
Phil Lee, Verneri Anttila, Hyejung Won1, Yen-Chen Anne Feng1  +603 moreInstitutions (10)
12 Dec 2019-Cell
TL;DR: Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes.

781 citations

Journal ArticleDOI
TL;DR: This Consensus Statement is one of the actions taken by the European Network Adult ADHD in order to support the clinician with research evidence and clinical experience from 18 European countries in which ADHD in adults is recognised and treated.
Abstract: Attention deficit hyperactivity disorder (ADHD) is among the most common psychiatric disorders of childhood that persists into adulthood in the majority of cases. The evidence on persistence poses several difficulties for adult psychiatry considering the lack of expertise for diagnostic assessment, limited treatment options and patient facilities across Europe. The European Network Adult ADHD, founded in 2003, aims to increase awareness of this disorder and improve knowledge and patient care for adults with ADHD across Europe. This Consensus Statement is one of the actions taken by the European Network Adult ADHD in order to support the clinician with research evidence and clinical experience from 18 European countries in which ADHD in adults is recognised and treated. Besides information on the genetics and neurobiology of ADHD, three major questions are addressed in this statement: (1) What is the clinical picture of ADHD in adults? (2) How can ADHD in adults be properly diagnosed? (3) How should ADHD in adults be effectively treated? ADHD often presents as an impairing lifelong condition in adults, yet it is currently underdiagnosed and treated in many European countries, leading to ineffective treatment and higher costs of illness. Expertise in diagnostic assessment and treatment of ADHD in adults must increase in psychiatry. Instruments for screening and diagnosis of ADHD in adults are available and appropriate treatments exist, although more research is needed in this age group.

775 citations

Journal ArticleDOI
Martine Hoogman1, Janita Bralten1, Derrek P. Hibar2, Maarten Mennes, Marcel P. Zwiers, Lizanne S.J. Schweren3, Kimm J. E. van Hulzen1, Sarah E. Medland4, Elena Shumskaya1, Neda Jahanshad2, Patrick de Zeeuw5, Eszter Szekely6, Gustavo Sudre6, Thomas Wolfers1, Alberdingk M.H. Onnink1, Janneke Dammers1, Jeanette C. Mostert1, Yolanda Vives-Gilabert, Gregor Kohls, Eileen Oberwelland, Jochen Seitz, Martin Schulte-Rüther, Sara Ambrosino5, Alysa E. Doyle7, Alysa E. Doyle8, Marie F. Høvik9, Margaretha Dramsdahl10, Leanne Tamm11, Theo G.M. van Erp12, Anders M. Dale13, Andrew J. Schork13, Annette Conzelmann14, Annette Conzelmann15, Kathrin C. Zierhut14, Ramona Baur14, Hazel McCarthy16, Yuliya N. Yoncheva17, Ana Cubillo18, Kaylita Chantiluke18, Mitul A. Mehta18, Yannis Paloyelis18, Sarah Hohmann19, Sarah Baumeister19, Ivanei E. Bramati, Paulo Mattos20, Fernanda Tovar-Moll20, Pamela K. Douglas21, Tobias Banaschewski19, Daniel Brandeis, Jonna Kuntsi18, Philip Asherson18, Katya Rubia18, Clare Kelly17, Clare Kelly16, Adriana Di Martino17, Michael P. Milham22, Michael P. Milham23, Francisco X. Castellanos17, Francisco X. Castellanos23, Thomas Frodl16, Thomas Frodl24, Mariam Zentis24, Klaus-Peter Lesch25, Klaus-Peter Lesch14, Andreas Reif26, Paul Pauli14, Terry L. Jernigan13, Jan Haavik27, Jan Haavik9, Kerstin J. Plessen, Astri J. Lundervold9, Kenneth Hugdahl27, Kenneth Hugdahl9, Larry J. Seidman8, Larry J. Seidman28, Joseph Biederman8, Nanda Rommelse1, Dirk J. Heslenfeld29, Catharina A. Hartman3, Pieter J. Hoekstra3, Jaap Oosterlaan29, Georg von Polier, Kerstin Konrad, Oscar Vilarroya30, Josep Antoni Ramos-Quiroga30, Joan Carles Soliva30, Sarah Durston5, Jan K. Buitelaar1, Stephen V. Faraone31, Stephen V. Faraone9, Philip Shaw6, Paul M. Thompson2, Barbara Franke1 
TL;DR: Lifespan analyses suggest that, in the absence of well powered longitudinal studies, the ENIGMA cross-sectional sample across six decades of ages provides a means to generate hypotheses about lifespan trajectories in brain phenotypes.

749 citations


Cited by
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Journal Article
TL;DR: For the next few weeks the course is going to be exploring a field that’s actually older than classical population genetics, although the approach it’ll be taking to it involves the use of population genetic machinery.
Abstract: So far in this course we have dealt entirely with the evolution of characters that are controlled by simple Mendelian inheritance at a single locus. There are notes on the course website about gametic disequilibrium and how allele frequencies change at two loci simultaneously, but we didn’t discuss them. In every example we’ve considered we’ve imagined that we could understand something about evolution by examining the evolution of a single gene. That’s the domain of classical population genetics. For the next few weeks we’re going to be exploring a field that’s actually older than classical population genetics, although the approach we’ll be taking to it involves the use of population genetic machinery. If you know a little about the history of evolutionary biology, you may know that after the rediscovery of Mendel’s work in 1900 there was a heated debate between the “biometricians” (e.g., Galton and Pearson) and the “Mendelians” (e.g., de Vries, Correns, Bateson, and Morgan). Biometricians asserted that the really important variation in evolution didn’t follow Mendelian rules. Height, weight, skin color, and similar traits seemed to

9,847 citations

Journal ArticleDOI
06 Jun 1986-JAMA
TL;DR: The editors have done a masterful job of weaving together the biologic, the behavioral, and the clinical sciences into a single tapestry in which everyone from the molecular biologist to the practicing psychiatrist can find and appreciate his or her own research.
Abstract: I have developed "tennis elbow" from lugging this book around the past four weeks, but it is worth the pain, the effort, and the aspirin. It is also worth the (relatively speaking) bargain price. Including appendixes, this book contains 894 pages of text. The entire panorama of the neural sciences is surveyed and examined, and it is comprehensive in its scope, from genomes to social behaviors. The editors explicitly state that the book is designed as "an introductory text for students of biology, behavior, and medicine," but it is hard to imagine any audience, interested in any fragment of neuroscience at any level of sophistication, that would not enjoy this book. The editors have done a masterful job of weaving together the biologic, the behavioral, and the clinical sciences into a single tapestry in which everyone from the molecular biologist to the practicing psychiatrist can find and appreciate his or

7,563 citations

Journal ArticleDOI
TL;DR: The theme of the volume is that it is human to have a long childhood which will leave a lifelong residue of emotional immaturity in man.
Abstract: Erik Eriksen is a remarkable individual. He has no college degrees yet is Professor of Human Development at Harvard University. He came to psychology via art, which explains why the reader will find him painting contexts and backgrounds rather than stating dull facts and concepts. He has been a training psychoanalyst for many years as well as a perceptive observer of cultural and social settings and their effect on growing up. This is not just a book on childhood. It is a panorama of our society. Anxiety in young children, apathy in American Indians, confusion in veterans of war, and arrogance in young Nazis are scrutinized under the psychoanalytic magnifying glass. The material is well written and devoid of technical jargon. The theme of the volume is that it is human to have a long childhood which will leave a lifelong residue of emotional immaturity in man. Primitive groups and

4,595 citations