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Evidence for Genetic Overlap Between Schizophrenia and Age at First Birth in Women.

https://arctichealth.org/en/permalink/ahliterature282521
Source
JAMA Psychiatry. 2016 May 01;73(5):497-505
Publication Type
Article
Date
May-01-2016
Author
Divya Mehta
Felix C Tropf
Jacob Gratten
Andrew Bakshi
Zhihong Zhu
Silviu-Alin Bacanu
Gibran Hemani
Patrik K E Magnusson
Nicola Barban
Tõnu Esko
Andres Metspalu
Harold Snieder
Bryan J Mowry
Kenneth S Kendler
Jian Yang
Peter M Visscher
John J McGrath
Melinda C Mills
Naomi R Wray
S Hong Lee
Ole A Andreassen
Elvira Bramon
Richard Bruggeman
Joseph D Buxbaum
Murray J Cairns
Rita M Cantor
C Robert Cloninger
David Cohen
Benedicto Crespo-Facorro
Ariel Darvasi
Lynn E DeLisi
Timothy Dinan
Srdjan Djurovic
Gary Donohoe
Elodie Drapeau
Valentina Escott-Price
Nelson B Freimer
Lyudmila Georgieva
Lieuwe de Haan
Frans A Henskens
Inge Joa
Antonio Julià
Andrey Khrunin
Bernard Lerer
Svetlana Limborska
Carmel M Loughland
Milan Macek
Sara Marsal
Robert W McCarley
Andrew M McIntosh
Andrew McQuillin
Bela Melegh
Patricia T Michie
Derek W Morris
Kieran C Murphy
Inez Myin-Germeys
Ann Olincy
Jim Van Os
Christos Pantelis
Danielle Posthuma
Digby Quested
Ulrich Schall
Rodney J Scott
Larry J Seidman
Draga Toncheva
Paul A Tooney
John Waddington
Daniel R Weinberger
Mark Weiser
Jing Qin Wu
Source
JAMA Psychiatry. 2016 May 01;73(5):497-505
Date
May-01-2016
Language
English
Publication Type
Article
Keywords
Adult
Alleles
Birth Order
Cohort Studies
Denmark
Female
Genetic Predisposition to Disease - genetics
Genome-Wide Association Study
Humans
Maternal Age
Phenotype
Pregnancy
Risk
Schizophrenia - genetics
Abstract
A recently published study of national data by McGrath et al in 2014 showed increased risk of schizophrenia (SCZ) in offspring associated with both early and delayed parental age, consistent with a U-shaped relationship. However, it remains unclear if the risk to the child is due to psychosocial factors associated with parental age or if those at higher risk for SCZ tend to have children at an earlier or later age.
To determine if there is a genetic association between SCZ and age at first birth (AFB) using genetically informative but independently ascertained data sets.
This investigation used multiple independent genome-wide association study data sets. The SCZ sample comprised 18?957 SCZ cases and 22?673 controls in a genome-wide association study from the second phase of the Psychiatric Genomics Consortium, and the AFB sample comprised 12?247 genotyped women measured for AFB from the following 4 community cohorts: Estonia (Estonian Genome Center Biobank, University of Tartu), the Netherlands (LifeLines Cohort Study), Sweden (Swedish Twin Registry), and the United Kingdom (TwinsUK). Schizophrenia genetic risk for each woman in the AFB community sample was estimated using genetic effects inferred from the SCZ genome-wide association study.
We tested if SCZ genetic risk was a significant predictor of response variables based on published polynomial functions that described the relationship between maternal age and SCZ risk in offspring in Denmark. We substituted AFB for maternal age in these functions, one of which was corrected for the age of the father, and found that the fit was superior for the model without adjustment for the father's age.
We observed a U-shaped relationship between SCZ risk and AFB in the community cohorts, consistent with the previously reported relationship between SCZ risk in offspring and maternal age when not adjusted for the age of the father. We confirmed that SCZ risk profile scores significantly predicted the response variables (coefficient of determination R2?=?1.1E-03, P?=?4.1E-04), reflecting the published relationship between maternal age and SCZ risk in offspring by McGrath et al in 2014.
This study provides evidence for a significant overlap between genetic factors associated with risk of SCZ and genetic factors associated with AFB. It has been reported that SCZ risk associated with increased maternal age is explained by the age of the father and that de novo mutations that occur more frequently in the germline of older men are the underlying causal mechanism. This explanation may need to be revised if, as suggested herein and if replicated in future studies, there is also increased genetic risk of SCZ in older mothers.
PubMed ID
27007234 View in PubMed
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Genetic and environmental factors affecting self-rated health from age 16-25: a longitudinal study of Finnish twins.

https://arctichealth.org/en/permalink/ahliterature167932
Source
Behav Genet. 2007 Mar;37(2):326-33
Publication Type
Article
Date
Mar-2007
Author
Karri Silventoinen
Danielle Posthuma
Eero Lahelma
Richard J Rose
Jaakko Kaprio
Author Affiliation
Department of Public Health, University of Helsinki, P.O. Box 41, Mannerheimintie 172, FIN-00014, Helsinki, Finland. karri.silventoinen@helsinki.fi
Source
Behav Genet. 2007 Mar;37(2):326-33
Date
Mar-2007
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Environment
Female
Finland
Genetics, Medical
Health status
Humans
Longitudinal Studies
Male
Models, Genetic
Questionnaires
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Abstract
We analyzed genetic and environmental determinants of self-rated health and its change from adolescence to early adulthood. Questionnaires were mailed to Finnish twins born 1975-1979 at ages 16, 17, 18 1/2 and, on average, 25 years of age (N=2465 complete twin pairs). The data were analyzed using quantitative genetic methods for twin data by the Mx statistical package. Heritability of self-rated health was greatest at age 16 (63%, 95% confidence intervals (CI) 56-67%, men and women together) and declined steadily to age 25 (33%, 95% CI 25-41%). The residual variation was due to unshared environments. Health ratings at different ages were modestly correlated (r=0.33-0.61). These correlations were mainly due to genetic factors, but unshared environment also contributed to them. An important challenge for further research is to identify environmental influences contributing to self-rated health independently of, or in interaction with, genetic factors.
PubMed ID
16906466 View in PubMed
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Genome-wide association analysis identifies 13 new risk loci for schizophrenia.

https://arctichealth.org/en/permalink/ahliterature107798
Source
Nat Genet. 2013 Oct;45(10):1150-9
Publication Type
Article
Date
Oct-2013
Author
Stephan Ripke
Colm O'Dushlaine
Kimberly Chambert
Jennifer L Moran
Anna K Kähler
Susanne Akterin
Sarah E Bergen
Ann L Collins
James J Crowley
Menachem Fromer
Yunjung Kim
Sang Hong Lee
Patrik K E Magnusson
Nick Sanchez
Eli A Stahl
Stephanie Williams
Naomi R Wray
Kai Xia
Francesco Bettella
Anders D Borglum
Brendan K Bulik-Sullivan
Paul Cormican
Nick Craddock
Christiaan de Leeuw
Naser Durmishi
Michael Gill
Vera Golimbet
Marian L Hamshere
Peter Holmans
David M Hougaard
Kenneth S Kendler
Kuang Lin
Derek W Morris
Ole Mors
Preben B Mortensen
Benjamin M Neale
Francis A O'Neill
Michael J Owen
Milica Pejovic Milovancevic
Danielle Posthuma
John Powell
Alexander L Richards
Brien P Riley
Douglas Ruderfer
Dan Rujescu
Engilbert Sigurdsson
Teimuraz Silagadze
August B Smit
Hreinn Stefansson
Stacy Steinberg
Jaana Suvisaari
Sarah Tosato
Matthijs Verhage
James T Walters
Douglas F Levinson
Pablo V Gejman
Claudine Laurent
Bryan J Mowry
Michael C O'Donovan
Ann E Pulver
Sibylle G Schwab
Dieter B Wildenauer
Frank Dudbridge
Jianxin Shi
Margot Albus
Madeline Alexander
Dominique Campion
David Cohen
Dimitris Dikeos
Jubao Duan
Peter Eichhammer
Stephanie Godard
Mark Hansen
F Bernard Lerer
Kung-Yee Liang
Wolfgang Maier
Jacques Mallet
Deborah A Nertney
Gerald Nestadt
Nadine Norton
George N Papadimitriou
Robert Ribble
Alan R Sanders
Jeremy M Silverman
Dermot Walsh
Nigel M Williams
Brandon Wormley
Maria J Arranz
Steven Bakker
Stephan Bender
Elvira Bramon
David Collier
Benedicto Crespo-Facorro
Jeremy Hall
Conrad Iyegbe
Assen Jablensky
Rene S Kahn
Luba Kalaydjieva
Stephen Lawrie
Cathryn M Lewis
Don H Linszen
Ignacio Mata
Andrew McIntosh
Robin M Murray
Roel A Ophoff
Jim Van Os
Muriel Walshe
Matthias Weisbrod
Durk Wiersma
Peter Donnelly
Ines Barroso
Jenefer M Blackwell
Matthew A Brown
Juan P Casas
Aiden P Corvin
Panos Deloukas
Audrey Duncanson
Janusz Jankowski
Hugh S Markus
Christopher G Mathew
Colin N A Palmer
Robert Plomin
Anna Rautanen
Stephen J Sawcer
Richard C Trembath
Ananth C Viswanathan
Nicholas W Wood
Chris C A Spencer
Gavin Band
Céline Bellenguez
Colin Freeman
Garrett Hellenthal
Eleni Giannoulatou
Matti Pirinen
Richard D Pearson
Amy Strange
Zhan Su
Damjan Vukcevic
Cordelia Langford
Sarah E Hunt
Sarah Edkins
Rhian Gwilliam
Hannah Blackburn
Suzannah J Bumpstead
Serge Dronov
Matthew Gillman
Emma Gray
Naomi Hammond
Alagurevathi Jayakumar
Owen T McCann
Jennifer Liddle
Simon C Potter
Radhi Ravindrarajah
Michelle Ricketts
Avazeh Tashakkori-Ghanbaria
Matthew J Waller
Paul Weston
Sara Widaa
Pamela Whittaker
Mark I McCarthy
Kari Stefansson
Edward Scolnick
Shaun Purcell
Steven A McCarroll
Pamela Sklar
Christina M Hultman
Patrick F Sullivan
Author Affiliation
1] Analytical and Translational Genetics Unit, Massachusetts General Hospital, Boston, Massachusetts, USA. [2] Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA. [3].
Source
Nat Genet. 2013 Oct;45(10):1150-9
Date
Oct-2013
Language
English
Publication Type
Article
Keywords
Case-Control Studies
Female
Genetic Predisposition to Disease
Genome-Wide Association Study
Humans
Male
Polymorphism, Single Nucleotide
Schizophrenia - genetics
Sweden
Abstract
Schizophrenia is an idiopathic mental disorder with a heritable component and a substantial public health impact. We conducted a multi-stage genome-wide association study (GWAS) for schizophrenia beginning with a Swedish national sample (5,001 cases and 6,243 controls) followed by meta-analysis with previous schizophrenia GWAS (8,832 cases and 12,067 controls) and finally by replication of SNPs in 168 genomic regions in independent samples (7,413 cases, 19,762 controls and 581 parent-offspring trios). We identified 22 loci associated at genome-wide significance; 13 of these are new, and 1 was previously implicated in bipolar disorder. Examination of candidate genes at these loci suggests the involvement of neuronal calcium signaling. We estimate that 8,300 independent, mostly common SNPs (95% credible interval of 6,300-10,200 SNPs) contribute to risk for schizophrenia and that these collectively account for at least 32% of the variance in liability. Common genetic variation has an important role in the etiology of schizophrenia, and larger studies will allow more detailed understanding of this disorder.
Notes
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PubMed ID
23974872 View in PubMed
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Meta-analysis of four new genome scans for lipid parameters and analysis of positional candidates in positive linkage regions.

https://arctichealth.org/en/permalink/ahliterature53137
Source
Eur J Hum Genet. 2005 Oct;13(10):1143-53
Publication Type
Article
Date
Oct-2005
Author
Bastiaan T Heijmans
Marian Beekman
Hein Putter
Nico Lakenberg
Henk Jan van der Wijk
John B Whitfield
Daniëlle Posthuma
Nancy L Pedersen
Nicholas G Martin
Dorret I Boomsma
P Eline Slagboom
Author Affiliation
Molecular Epidemiology, Leiden University Medical Centre, Leiden, The Netherlands. b.t.heijmans@lumc.nl
Source
Eur J Hum Genet. 2005 Oct;13(10):1143-53
Date
Oct-2005
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Apolipoprotein A-I - blood
Apolipoproteins B - blood
Australia
Chromosome Mapping - methods
Female
Genome, Human
Humans
Lipoproteins, HDL Cholesterol - blood
Lipoproteins, LDL Cholesterol - blood
Lod Score
Male
Middle Aged
Netherlands
Quantitative Trait Loci
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Sweden
Twins, Dizygotic - genetics
Abstract
Lipid levels in plasma strongly influence the risk for coronary heart disease. To localise and subsequently identify genes affecting lipid levels, we performed four genome-wide linkage scans followed by combined linkage/association analysis. Genome-scans were performed in 701 dizygotic twin pairs from four samples with data on plasma levels of HDL- and LDL-cholesterol and their major protein constituents, apolipoprotein AI (ApoAI) and Apolipoprotein B (ApoB). To maximise power, the genome scans were analysed simultaneously using a well-established meta-analysis method that was newly applied to linkage analysis. Overall LOD scores were estimated using the means of the sample-specific quantitative trait locus (QTL) effects inversely weighted by the standard errors obtained using an inverse regression method. Possible heterogeneity was accounted for with a random effects model. Suggestive linkage for HDL-C was observed on 8p23.1 and 12q21.2 and for ApoAI on 1q21.3. For LDL-C and ApoB, linkage regions frequently coincided (2p24.1, 2q32.1, 19p13.2 and 19q13.31). Six of the putative QTLs replicated previous findings. After fine mapping, three maximum LOD scores mapped within 1 cM of major candidate genes, namely APOB (LOD=2.1), LDLR (LOD=1.9) and APOE (LOD=1.7). APOB haplotypes explained 27% of the QTL effect observed for LDL-C on 2p24.1 and reduced the LOD-score by 0.82. Accounting for the effect of the LDLR and APOE haplotypes did not change the LOD score close to the LDLR gene but abolished the linkage signal at the APOE gene. In conclusion, application of a new meta-analysis approach maximised the power to detect QTLs for lipid levels and improved the precision of their location estimate.
PubMed ID
16015283 View in PubMed
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