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Ancient genomes from Iceland reveal the making of a human population.

https://arctichealth.org/en/permalink/ahliterature294280
Source
Science. 2018 06 01; 360(6392):1028-1032
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
06-01-2018
Author
S Sunna Ebenesersdóttir
Marcela Sandoval-Velasco
Ellen D Gunnarsdóttir
Anuradha Jagadeesan
Valdís B Guðmundsdóttir
Elísabet L Thordardóttir
Margrét S Einarsdóttir
Kristjan H S Moore
Ásgeir Sigurðsson
Droplaug N Magnúsdóttir
Hákon Jónsson
Steinunn Snorradóttir
Eivind Hovig
Pål Møller
Ingrid Kockum
Tomas Olsson
Lars Alfredsson
Thomas F Hansen
Thomas Werge
Gianpiero L Cavalleri
Edmund Gilbert
Carles Lalueza-Fox
Joe W Walser
Steinunn Kristjánsdóttir
Shyam Gopalakrishnan
Lilja Árnadóttir
Ólafur Þ Magnússon
M Thomas P Gilbert
Kári Stefánsson
Agnar Helgason
Author Affiliation
deCODE Genetics/AMGEN, Inc., Reykjavik Iceland. sunna@decode.is kstefan@deocde.is agnar@decode.is.
Source
Science. 2018 06 01; 360(6392):1028-1032
Date
06-01-2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Biological Evolution
DNA, Ancient
Female
Founder Effect
Gene Pool
Genetic Drift
Genome, Human
Genotype
Humans
Iceland
Male
Phenotype
Population - genetics
Abstract
Opportunities to directly study the founding of a human population and its subsequent evolutionary history are rare. Using genome sequence data from 27 ancient Icelanders, we demonstrate that they are a combination of Norse, Gaelic, and admixed individuals. We further show that these ancient Icelanders are markedly more similar to their source populations in Scandinavia and the British-Irish Isles than to contemporary Icelanders, who have been shaped by 1100 years of extensive genetic drift. Finally, we report evidence of unequal contributions from the ancient founders to the contemporary Icelandic gene pool. These results provide detailed insights into the making of a human population that has proven extraordinarily useful for the discovery of genotype-phenotype associations.
Notes
CommentIn: Science. 2018 Jun 1;360(6392):964-965 PMID 29853673
PubMed ID
29853688 View in PubMed
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Association analysis of ANK3 gene variants in nordic bipolar disorder and schizophrenia case-control samples.

https://arctichealth.org/en/permalink/ahliterature130741
Source
Am J Med Genet B Neuropsychiatr Genet. 2011 Dec;156B(8):969-74
Publication Type
Article
Date
Dec-2011
Author
Martin Tesli
Pernille Koefoed
Lavinia Athanasiu
Morten Mattingsdal
Omar Gustafsson
Ingrid Agartz
Lars M Rimol
Andrew Brown
Katrine V Wirgenes
Lisa-Lena Smorr
Anna K Kähler
Thomas Werge
Ole Mors
Erling Mellerup
Erik G Jönsson
Ingrid Melle
Gunnar Morken
Srdjan Djurovic
Ole A Andreassen
Author Affiliation
Institute of Clinical Medicine, University of Oslo, Oslo, Norway. m.s.tesli@medisin.uio.no
Source
Am J Med Genet B Neuropsychiatr Genet. 2011 Dec;156B(8):969-74
Date
Dec-2011
Language
English
Publication Type
Article
Keywords
Ankyrins - genetics
Bipolar Disorder - genetics
Case-Control Studies
Female
Gene Frequency
Genetic Association Studies
Genetic Predisposition to Disease
Genetic Variation
Genotype
Humans
Iceland
Male
Polymorphism, Single Nucleotide
Scandinavia
Schizophrenia - genetics
Abstract
Genetic variants in ankyrin 3 (ANK3) have recently been shown to be associated with bipolar disorder (BD). We genotyped three ANK3 SNPs previously found to be associated with BD (rs10994336, rs1938526, and rs9804190) in a Scandinavian BD case-control sample (N = 854/2,614). Due to evidence of genetic overlap between BD and schizophrenia (SZ), we also genotyped these three SNPs in a Scandinavian SZ case-control sample (N = 1,073/2,919). Combining our Scandinavian samples with an Icelandic sample (N = 435 BD cases, 651 SZ cases, and 11,491 healthy controls), we found rs10994336 and rs9804190 to be nominally significantly associated with BD in this combined Nordic BD sample (N = 1,289/14,105). Nominal P was 0.015/0.018 (fixed/random effect) for rs10994336 (Bonferroni corrected P = 0.044/0.053) and 0.023 for rs9804190 (Bonferroni corrected P = 0.069). None of the SNPs were significantly associated with SZ in the combined Nordic SZ case-control sample (N = 1,724/14,410). These results further support that ANK3 is a susceptibility gene specific to BD and that more than one risk locus is involved.
PubMed ID
21972176 View in PubMed
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Association analysis of schizophrenia on 18 genes involved in neuronal migration: MDGA1 as a new susceptibility gene.

https://arctichealth.org/en/permalink/ahliterature157931
Source
Am J Med Genet B Neuropsychiatr Genet. 2008 Oct 5;147B(7):1089-100
Publication Type
Article
Date
Oct-5-2008
Author
Anna K Kähler
Srdjan Djurovic
Bettina Kulle
Erik G Jönsson
Ingrid Agartz
Håkan Hall
Stein Opjordsmoen
Klaus D Jakobsen
Thomas Hansen
Ingrid Melle
Thomas Werge
Vidar M Steen
Ole A Andreassen
Author Affiliation
TOP Project, Institute of Psychiatry, University of Oslo, Oslo, Norway. a.k.kahler@medisin.uio.no
Source
Am J Med Genet B Neuropsychiatr Genet. 2008 Oct 5;147B(7):1089-100
Date
Oct-5-2008
Language
English
Publication Type
Article
Keywords
Adult
Aged
Cell Adhesion - genetics
Cell Adhesion Molecules - genetics
Cell Movement - genetics
Female
GPI-Linked Proteins
Genetic Predisposition to Disease
Genotype
Humans
Linkage Disequilibrium
Male
Middle Aged
Nerve Tissue Proteins - metabolism
Neural Cell Adhesion Molecules
Neuroglia
Neurons - pathology
Polymorphism, Single Nucleotide
Scandinavia
Schizophrenia - genetics
Abstract
Several lines of evidence support the theory of schizophrenia (SZ) being a neurodevelopmental disorder. The structural, cytoarchitectural and functional brain abnormalities reported in patients with SZ, might be due to aberrant neuronal migration, since the final position of neurons affects neuronal function, morphology, and formation of synaptic connections. We have investigated the putative association between SZ and gene variants engaged in the neuronal migration process, by performing an association study on 839 cases and 1,473 controls of Scandinavian origin. Using a gene-wide approach, tagSNPs in 18 candidate genes have been genotyped, with gene products involved in the neuron-to-glial cell adhesion, interactions with the DISC1 protein and/or rearrangements of the cytoskeleton. Of the 289 markers tested, 19 markers located in genes MDGA1, RELN, ITGA3, DLX1, SPARCL1, and ASTN1, attained nominal significant P-values (P
PubMed ID
18384059 View in PubMed
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Association between a disrupted-in-schizophrenia 1 (DISC1) single nucleotide polymorphism and schizophrenia in a combined Scandinavian case-control sample.

https://arctichealth.org/en/permalink/ahliterature155007
Source
Schizophr Res. 2008 Dec;106(2-3):237-41
Publication Type
Article
Date
Dec-2008
Author
Peter Saetre
Ingrid Agartz
Alessandra De Franciscis
Per Lundmark
Srdjan Djurovic
Anna Kähler
Ole A Andreassen
Klaus D Jakobsen
Henrik B Rasmussen
Thomas Werge
Håkan Hall
Lars Terenius
Erik G Jönsson
Author Affiliation
Department of Clinical Neuroscience, HUBIN project, Karolinska Institutet and Hospital, R5:00, SE-171 76 Stockholm, Sweden. peter.saetre@ki.se
Source
Schizophr Res. 2008 Dec;106(2-3):237-41
Date
Dec-2008
Language
English
Publication Type
Article
Keywords
Adult
Case-Control Studies
Chromosome Mapping
European Continental Ancestry Group - genetics
Female
Gene Frequency
Genetic Predisposition to Disease - genetics
Genotype
Humans
Male
Middle Aged
Mutation - genetics
Nerve Tissue Proteins - genetics
Pedigree
Polymorphism, Single Nucleotide - genetics
Risk factors
Scandinavia - ethnology
Schizophrenia - genetics
Abstract
Disrupted-in-schizophrenia-1 (DISC1), located on chromosome 1q42.1, is linked to rare familial schizophrenia in a large Scottish family. The chromosomal translocation that segregates with the disease results in a truncated protein that impairs neurite outgrowth and proper development of the cerebral cortex, suggesting that lost DISC1 function may underlie neurodevelopmental dysfunction in schizophrenia. DISC1 has been associated with schizophrenia in multiple populations, but there is little evidence of convergence across populations. In the present case-control study three Scandinavian samples of 837 individuals affected with schizophrenia and 1473 controls, were used in an attempt to replicate previously reported associations between single nucleotide polymorphisms (SNPs) in DISC1 and schizophrenia. No SNP with allele frequency above 10% was significantly associated with the disease after correction for multiple testing. However, the minor allele of rs3737597 (frequency 2%) in the 3'-untranslated region (UTR), previously identified as a risk allele in Finnish families, was significantly and consistently associated with the disorder across the three samples, (p-value corrected for multiple testing was 0.002). Our results suggest that a relatively uncommon DISC1 mutation, which increases the susceptibility for schizophrenia may be segregating in the Scandinavian population, and support the view that common DISC1 SNP alleles are unlikely to account for a substantial proportion of the genetic risk of the disease across populations of European descent.
PubMed ID
18818052 View in PubMed
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Association of AADAC Deletion and Gilles de la Tourette Syndrome in a Large European Cohort.

https://arctichealth.org/en/permalink/ahliterature277219
Source
Biol Psychiatry. 2016 Mar 1;79(5):383-91
Publication Type
Article
Date
Mar-1-2016
Author
Birgitte Bertelsen
Hreinn Stefánsson
Lars Riff Jensen
Linea Melchior
Nanette Mol Debes
Camilla Groth
Liselotte Skov
Thomas Werge
Iordanis Karagiannidis
Zsanett Tarnok
Csaba Barta
Peter Nagy
Luca Farkas
Karen Brøndum-Nielsen
Renata Rizzo
Mariangela Gulisano
Dan Rujescu
Lambertus A Kiemeney
Sarah Tosato
Muhammad Sulaman Nawaz
Andres Ingason
Unnur Unnsteinsdottir
Stacy Steinberg
Pétur Ludvigsson
Kari Stefansson
Andreas Walter Kuss
Peristera Paschou
Danielle Cath
Pieter J Hoekstra
Kirsten Müller-Vahl
Manfred Stuhrmann
Asli Silahtaroglu
Rolph Pfundt
Zeynep Tümer
Source
Biol Psychiatry. 2016 Mar 1;79(5):383-91
Date
Mar-1-2016
Language
English
Publication Type
Article
Keywords
Adult
Animals
Attention Deficit Disorder with Hyperactivity - genetics
Cohort Studies
Comorbidity
DNA Copy Number Variations - genetics
Denmark
Exons
Female
Genotyping Techniques
Germany
Humans
Hungary
Iceland
Italy
Male
Mice
Netherlands
Sequence Deletion - genetics
Tourette Syndrome - genetics
Abstract
Gilles de la Tourette syndrome (GTS) is a complex neuropsychiatric disorder with a strong genetic influence where copy number variations are suggested to play a role in disease pathogenesis. In a previous small-scale copy number variation study of a GTS cohort (n = 111), recurrent exon-affecting microdeletions of four genes, including the gene encoding arylacetamide deacetylase (AADAC), were observed and merited further investigations.
We screened a Danish cohort of 243 GTS patients and 1571 control subjects for submicroscopic deletions and duplications of these four genes. The most promising candidate gene, AADAC, identified in this Danish discovery sample was further investigated in cohorts from Iceland, the Netherlands, Hungary, Germany, and Italy, and a final meta-analysis, including a total of 1181 GTS patients and 118,730 control subjects from these six European countries, was performed. Subsequently, expression of the candidate gene in the central nervous system was investigated using human and mouse brain tissues.
In the Danish cohort, we identified eight patients with overlapping deletions of AADAC. Investigation of the additional five countries showed a significant association between the AADAC deletion and GTS, and a final meta-analysis confirmed the significant association (p = 4.4 ? 10(-4); odds ratio = 1.9; 95% confidence interval = 1.33-2.71). Furthermore, RNA in situ hybridization and reverse transcription-polymerase chain reaction studies revealed that AADAC is expressed in several brain regions previously implicated in GTS pathology.
AADAC is a candidate susceptibility factor for GTS and the present findings warrant further genomic and functional studies to investigate the role of this gene in the pathogenesis of GTS.
Notes
Comment In: Biol Psychiatry. 2016 Mar 1;79(5):341-226847659
PubMed ID
26444075 View in PubMed
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Association of MCTP2 gene variants with schizophrenia in three independent samples of Scandinavian origin (SCOPE).

https://arctichealth.org/en/permalink/ahliterature152584
Source
Psychiatry Res. 2009 Aug 15;168(3):256-8
Publication Type
Article
Date
Aug-15-2009
Author
Srdjan Djurovic
Stephanie Le Hellard
Anna K Kähler
Erik G Jönsson
Ingrid Agartz
Vidar M Steen
Håkan Hall
August G Wang
Henrik B Rasmussen
Ingrid Melle
Thomas Werge
Ole A Andreassen
Author Affiliation
Institute of Psychiatry, University of Oslo, Norway. srdjan.djurovic@medisin.uio.no
Source
Psychiatry Res. 2009 Aug 15;168(3):256-8
Date
Aug-15-2009
Language
English
Publication Type
Article
Keywords
Female
Gene Frequency
Genetic Predisposition to Disease
Genome-Wide Association Study
Genotype
Humans
Male
Membrane Proteins - genetics
Polymorphism, Single Nucleotide - genetics
Scandinavia
Schizophrenia - genetics
Abstract
The MCTP2 gene is involved in intercellular signal transduction and synapse function. We genotyped 37 tagging SNPs across the MCTP2 gene to study a possible association with schizophrenia in three independent Scandinavian samples. We report, for the first time, a possible involvement of MCTP2 as a potential novel susceptibility gene for schizophrenia.
PubMed ID
19223264 View in PubMed
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Association study of PDE4B gene variants in Scandinavian schizophrenia and bipolar disorder multicenter case-control samples.

https://arctichealth.org/en/permalink/ahliterature151647
Source
Am J Med Genet B Neuropsychiatr Genet. 2010 Jan 5;153B(1):86-96
Publication Type
Article
Date
Jan-5-2010
Author
Anna K Kähler
Mona K Otnaess
Katrine V Wirgenes
Thomas Hansen
Erik G Jönsson
Ingrid Agartz
HÃ¥kan Hall
Thomas Werge
Gunnar Morken
Ole Mors
Erling Mellerup
Henrik Dam
Pernille Koefod
Ingrid Melle
Vidar M Steen
Ole A Andreassen
Srdjan Djurovic
Author Affiliation
Institute of Psychiatry, University of Oslo, Oslo, Norway. a.k.kahler@medisin.uio.no
Source
Am J Med Genet B Neuropsychiatr Genet. 2010 Jan 5;153B(1):86-96
Date
Jan-5-2010
Language
English
Publication Type
Article
Keywords
Bipolar Disorder - enzymology - genetics
Case-Control Studies
Cyclic Nucleotide Phosphodiesterases, Type 4 - genetics
Female
Haplotypes
Humans
Male
Polymorphism, Single Nucleotide
Scandinavia
Schizophrenia - enzymology - genetics
Abstract
The phosphodiesterase 4B (PDE4B), which is involved in cognitive function in animal models, is a candidate susceptibility gene for schizophrenia (SZ) and bipolar disorder (BP). Variations in PDE4B have previously been associated with SZ, with a suggested gender-specific effect. We have genotyped and analyzed 40 and 72 tagging single nucleotide polymorphisms (tagSNPs) in SZ and BP multicenter samples, respectively, from the Scandinavian Collaboration on Psychiatric Etiology (SCOPE), involving 837 SZ cases and 1,473 controls plus 594 BP cases and 1,421 partly overlapping controls. Six and 16 tagSNPs were nominally associated (0.0005
PubMed ID
19350560 View in PubMed
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Brain expressed microRNAs implicated in schizophrenia etiology.

https://arctichealth.org/en/permalink/ahliterature161432
Source
PLoS One. 2007;2(9):e873
Publication Type
Article
Date
2007
Author
Thomas Hansen
Line Olsen
Morten Lindow
Klaus D Jakobsen
Henrik Ullum
Erik Jonsson
Ole A Andreassen
Srdjan Djurovic
Ingrid Melle
Ingrid Agartz
Håkan Hall
Sally Timm
August G Wang
Thomas Werge
Author Affiliation
Research Institute of Biological Psychiatry, Sct. Hans Hospital, Roskilde, Denmark.
Source
PLoS One. 2007;2(9):e873
Date
2007
Language
English
Publication Type
Article
Keywords
Adult
Brain - metabolism
Case-Control Studies
Denmark
Female
Genotype
Humans
Male
MicroRNAs - genetics
Middle Aged
Norway
Schizophrenia - genetics
Sweden
Abstract
Protein encoding genes have long been the major targets for research in schizophrenia genetics. However, with the identification of regulatory microRNAs (miRNAs) as important in brain development and function, miRNAs genes have emerged as candidates for schizophrenia-associated genetic factors. Indeed, the growing understanding of the regulatory properties and pleiotropic effects that miRNA have on molecular and cellular mechanisms, suggests that alterations in the interactions between miRNAs and their mRNA targets may contribute to phenotypic variation.
We have studied the association between schizophrenia and genetic variants of miRNA genes associated with brain-expression using a case-control study design on three Scandinavian samples. Eighteen known SNPs within or near brain-expressed miRNAs in three samples (Danish, Swedish and Norwegian: 420/163/257 schizophrenia patients and 1006/177/293 control subjects), were analyzed. Subsequently, joint analysis of the three samples was performed on SNPs showing marginal association. Two SNPs rs17578796 and rs1700 in hsa-mir-206 (mir-206) and hsa-mit-198 (mir-198) showed nominal significant allelic association to schizophrenia in the Danish and Norwegian sample respectively (P = 0.0021 & p = 0.038), of which only rs17578796 was significant in the joint sample. In-silico analysis revealed that 8 of the 15 genes predicted to be regulated by both mir-206 and mir-198, are transcriptional targets or interaction partners of the JUN, ATF2 and TAF1 connected in a tight network. JUN and two of the miRNA targets (CCND2 and PTPN1) in the network have previously been associated with schizophrenia.
We found nominal association between brain-expressed miRNAs and schizophrenia for rs17578796 and rs1700 located in mir-206 and mir-198 respectively. These two miRNAs have a surprising large number (15) of targets in common, eight of which are also connected by the same transcription factors.
Notes
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PubMed ID
17849003 View in PubMed
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Combinations of Genetic Data Present in Bipolar Patients, but Absent in Control Persons.

https://arctichealth.org/en/permalink/ahliterature273873
Source
PLoS One. 2015;10(11):e0143432
Publication Type
Article
Date
2015
Author
Erling Mellerup
Ole A Andreassen
Bente Bennike
Henrik Dam
Srdjan Djurovic
Thomas Hansen
Martin Balslev Jorgensen
Lars Vedel Kessing
Pernille Koefoed
Ingrid Melle
Ole Mors
Thomas Werge
Gert Lykke Moeller
Source
PLoS One. 2015;10(11):e0143432
Date
2015
Language
English
Publication Type
Article
Keywords
Bipolar Disorder - genetics
Case-Control Studies
Cluster analysis
Denmark
Genetic Predisposition to Disease
Genotype
Humans
Models, Genetic
Models, Statistical
Norway
Polymorphism, Single Nucleotide
Risk factors
Abstract
The main objective of the study was to find combinations of genetic variants significantly associated with bipolar disorder. In a previous study of bipolar disorder, combinations of three single nucleotide polymorphism (SNP) genotypes taken from 803 SNPs were analyzed, and four clusters of combinations were found to be significantly associated with bipolar disorder. In the present study, combinations of four SNP genotypes taken from the same 803 SNPs were analyzed, and one cluster of combinations was found to be significantly associated with bipolar disorder. Combinations from the new cluster and from the four previous clusters were identified in the genomes of 209 of the 607 patients in the study whereas none of the 1355 control participants had any of these combinations in their genome.
Notes
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PubMed ID
26587987 View in PubMed
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Copy number variations in affective disorders and meta-analysis.

https://arctichealth.org/en/permalink/ahliterature135730
Source
Psychiatr Genet. 2011 Dec;21(6):319-22
Publication Type
Article
Date
Dec-2011
Author
Line Olsen
Thomas Hansen
Srdjan Djurovic
Eva Haastrup
Anders Albrecthsen
Louise K E Hoeffding
Anna Secher
Omar Gustafsson
Klaus D Jakobsen
Finn C Nielsen
Henrik Ullum
Gunnar Morken
Ingrid Agartz
Ingrid Melle
Ulrik Gether
Ole A Andreassen
Thomas Werge
Author Affiliation
Institute for Biological Psychiatry, Mental Health Centre Sct. Hans, Roskilde, Norway.
Source
Psychiatr Genet. 2011 Dec;21(6):319-22
Date
Dec-2011
Language
English
Publication Type
Article
Keywords
Bipolar Disorder - genetics
Case-Control Studies
DNA Copy Number Variations - genetics
Genetic Predisposition to Disease
Humans
Mood Disorders - genetics
Scandinavia
Abstract
In two recent studies 10 copy number variants (CNV) were found to be overrepresented either among patients suffering from affective disorders in an Amish family or in the Wellcome Trust Case-Control Consortium study. Here, we investigate if these variants are associated with affective disorders in a combined analysis of three case-control samples from Denmark, Norway and Iceland. A total of 1897 cases (n=1223 unipolar and n=463 bipolar) and 11 231 controls were analyzed for CNVs at the 10 genomic loci, but we found no combined association between these CNVs and affective disorders.
PubMed ID
21451435 View in PubMed
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33 records – page 1 of 4.