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5-HT2C receptor and MAO-A interaction analysis: no association with suicidal behaviour in bipolar patients.

https://arctichealth.org/en/permalink/ahliterature157011
Source
Eur Arch Psychiatry Clin Neurosci. 2008 Oct;258(7):428-33
Publication Type
Article
Date
Oct-2008
Author
Vincenzo De Luca
Subi Tharmaligam
John Strauss
James L Kennedy
Author Affiliation
Dept. of Psychiatry, University of Toronto, 250 College Street, R-30, Toronto (ON), Canada M5T 1R8. vincenzo_deluca@camh.net
Source
Eur Arch Psychiatry Clin Neurosci. 2008 Oct;258(7):428-33
Date
Oct-2008
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Bipolar Disorder - genetics - psychology
Canada
Family Health
Female
Gene Frequency
Genes, X-Linked
Genetic Predisposition to Disease
Genotype
Haplotypes
Humans
Male
Middle Aged
Monoamine Oxidase - genetics
Nuclear Family
Polymorphism, Single Nucleotide
Receptor, Serotonin, 5-HT2C - genetics
Suicide, Attempted - psychology
Young Adult
Abstract
The serotonin 2C (HTR2C) receptor has been implicated in suicide-related behaviours, however there are not many studies to date about HTR2C and suicidality. We studied HTR2C haplotypes in suicide attempters, where our sample composed of 306 families with at least one member affected by bipolar disorder. HTR2C (Cys23Ser and a common STR in the promoter) variants were analyzed with respect to attempter status and the severity of suicidal behaviour. The X-linked haplotype analysis in relation to suicide attempt did not reveal any significant association. Furthermore, we performed a particular gene-gene interaction for the X-linked serotonergic genes (HTR2C and MAOA), and found no association among this intergenic haplotype combination and suicidal behaviour in bipolar disorder.
PubMed ID
18504633 View in PubMed
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Age of onset in affective disorder: its correlation with hereditary and psychosocial factors.

https://arctichealth.org/en/permalink/ahliterature46188
Source
J Affect Disord. 2000 Aug;59(2):139-48
Publication Type
Article
Date
Aug-2000
Author
L. Johnson
G. Andersson-Lundman
A. Aberg-Wistedt
A A Mathé
Author Affiliation
Department of Clinical Neuroscience, Section of Psychiatry, St. Göran's Hospital, Karolinska Institute, Box 12500, S-11281, Stockholm, Sweden. lars.johnson@pskl.csso.sll.se
Source
J Affect Disord. 2000 Aug;59(2):139-48
Date
Aug-2000
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Aged
Bipolar Disorder - genetics - psychology
Depressive Disorder - genetics - psychology
Female
Genetic Predisposition to Disease
Humans
Life Change Events
Male
Middle Aged
Models, Psychological
Mood Disorders - epidemiology - genetics - psychology
Parent-Child Relations
Recurrence
Retrospective Studies
Stress, Psychological - complications
Sweden - epidemiology
Abstract
BACKGROUND: Affective disorders probably have a multifactorial aetiology, both biological and psychosocial factors may be of importance at onset as well as at relapses. The aim of the study was to investigate how the age of onset of bipolar and unipolar disorder relates to family history of affective disorder, early parental separation and life events. A second purpose of this study was to analyze the importance of life events preceding the first and subsequent episodes of affective disorder. METHODS: The case records of 282 patients (161 females/121 males; mean age 56) were investigated. They all had a DSM-IV based diagnosis of either bipolar I/II (67%) or unipolar (33%) disorder. Variables, such as family history, early parental loss and life events according to Paykel life events scale, were examined. RESULTS: We found a significantly lower age of onset in bipolar patients with a family history of affective disorder (28.9 vs. 33.9 years). Bipolar patients with preceding life events had a higher age of onset (33.1 vs. 28.3 years). Moreover, bipolar patients with heredity, had less life events at onset. For the bipolar, as well as the unipolar group, life stressors more frequently preceded the first episode of affective disorder than the subsequent episodes. Limitations: The major limitation of this study is the retrospective approach, with e.g. difficulties to decide whether a life event plays a role in aetiology of affective disorder or is its consequence. CONCLUSIONS: Bipolar patients with high constitutional vulnerability have an earlier age of onset and need less stress factors to become ill. Better knowledge about the stress- and the vulnerability-factors in affective disorder might contribute to development of individually tailored therapeutic strategies in future.
PubMed ID
10837882 View in PubMed
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Anticipation in Swedish families with bipolar affective disorder.

https://arctichealth.org/en/permalink/ahliterature217460
Source
J Med Genet. 1994 Sep;31(9):686-9
Publication Type
Article
Date
Sep-1994
Author
P O Nylander
C. Engström
J. Chotai
J. Wahlström
R. Adolfsson
Author Affiliation
Department of Psychiatry, University of Umeå, Sweden.
Source
J Med Genet. 1994 Sep;31(9):686-9
Date
Sep-1994
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age of Onset
Bipolar Disorder - genetics
Female
Humans
Male
Middle Aged
Pedigree
Regression Analysis
Sweden
Abstract
Anticipation describes an inheritance pattern within a pedigree with an increase in disease severity or decrease in age at onset or both in successive generations. The phenomenon of anticipation has recently been shown to be correlated with the expansion of trinucleotide repeat sequences in different disorders. We have studied differences of age at onset and disease severity between two generations in 14 families with unilinear inheritance of bipolar affective disorder (BPAD). There was a significant difference in age at onset (p
Notes
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PubMed ID
7815436 View in PubMed
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Association analyses suggest GPR24 as a shared susceptibility gene for bipolar affective disorder and schizophrenia.

https://arctichealth.org/en/permalink/ahliterature169019
Source
Am J Med Genet B Neuropsychiatr Genet. 2006 Jul 5;141B(5):524-33
Publication Type
Article
Date
Jul-5-2006
Author
J E Severinsen
T D Als
H. Binderup
T A Kruse
A G Wang
M. Vang
W J Muir
D H R Blackwood
O. Mors
A D Børglum
Author Affiliation
Institute of Human Genetics, University of Aarhus, Aarhus, Denmark.
Source
Am J Med Genet B Neuropsychiatr Genet. 2006 Jul 5;141B(5):524-33
Date
Jul-5-2006
Language
English
Publication Type
Article
Keywords
Bipolar Disorder - genetics
Case-Control Studies
Denmark
Female
Gene Frequency
Genetic Predisposition to Disease - genetics
Genotype
Haplotypes
Humans
Linkage Disequilibrium
Male
Pedigree
Polymorphism, Single Nucleotide
Receptors, Somatostatin - genetics
Schizophrenia - genetics
Scotland
Abstract
Linkage analyses suggest that chromosome 22q12-13 may harbor a shared susceptibility locus for bipolar affective disorder (BPD) and schizophrenia (SZ). In a study of a sample from the Faeroe Islands we have previously reported association between both disorders and microsatellite markers in a 3.6 cM segment on 22q13. The present study investigated three candidate genes located in this segment: GPR24, ADSL, and ST13. Nine SNPs located in these genes and one microsatellite marker (D22S279) were applied in an association analysis of two samples: an extension of the previously analyzed Faeroese sample comprising 28 distantly related cases (17 BPD, 11 SZ subjects) and 44 controls, and a Scottish sample including 162 patients with BPD, 103 with SZ, and 200 controls. In both samples significant associations were observed in both disorders with predominantly GPR24 SNPs and haplotypes. In the Faeroese sample overall P-values of 0.0009, 0.0054, and 0.0023 were found for haplotypes in BPD, SZ, and combined cases, respectively, and in the Scottish sample overall P-values of 0.0003, 0.0005, and 0.016 were observed for similar groupings. Specific haplotypes showed associations with lowest P-values of 7 x 10(-5) and 0.0006 in the combined group of cases from the Faeroe Islands and Scotland, respectively. The G protein-coupled receptor 24 encoded by GPR24 binds melanin-concentrating hormone (MCH) and has been implicated with feeding behavior, energy metabolism, and regulation of stress and mood. To our knowledge this is the first study reporting association between GPR24 and BPD and SZ, suggesting that GPR24 variants may confer susceptibility to both disorders.
PubMed ID
16741940 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
Less detail
Source
Am J Med Genet. 1999 Jun 18;88(3):255-9
Publication Type
Conference/Meeting Material
Date
Jun-18-1999
Author
S D Detera-Wadleigh
Author Affiliation
National Institute of Mental Health Intramural Program, National Institutes of Health, Bethesda, Maryland 20892, USA.
Source
Am J Med Genet. 1999 Jun 18;88(3):255-9
Date
Jun-18-1999
Language
English
Publication Type
Conference/Meeting Material
Keywords
Alcoholism - genetics
Bipolar Disorder - genetics
Chromosomes, Human, Pair 12
Chromosomes, Human, Pair 16
Genetic Predisposition to Disease
Humans
Linkage (Genetics)
Panic Disorder - genetics
Schizophrenia - genetics
Abstract
Recent linkage results independently derived from a large French Canadian pedigree and Danish kindreds coupled with supportive data from other studies provide compelling evidence for a bipolar disorder susceptibility locus on chromosome 12q23-q24. The idea is further strengthened by the finding that Darier's disease, which maps to this region, has been shown to cosegregate with affective disorder in a family. This linkage finding, however, was not supported in other independent genome scans. On chromosome 16, bipolar families from Denmark exhibited suggestive linkage with D16S510, on 16p13. Multipoint nonparametric analysis on the NIMH Genetics Initiative bipolar pedigrees yielded increased allele sharing that maximized approximately 18 cM proximal to the latter locus. In contrast, evidence of linkage was not detected in other panels of bipolar families that were presented. At 16p13, a maximum multipoint lod score of 4 for a latent class-derived phenotype that has aspects of alcohol dependence was found in a genome scan of 105 families from the Collaborative Study of the Genetics of Alcoholism, identifying a potential vulnerability locus.
PubMed ID
10374740 View in PubMed
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Cognitive endophenotypes inform genome-wide expression profiling in schizophrenia.

https://arctichealth.org/en/permalink/ahliterature275391
Source
Neuropsychology. 2016 Jan;30(1):40-52
Publication Type
Article
Date
Jan-2016
Author
Amanda B Zheutlin
Rachael W Viehman
Rebecca Fortgang
Jacqueline Borg
Desmond J Smith
Jaana Suvisaari
Sebastian Therman
Christina M Hultman
Tyrone D Cannon
Source
Neuropsychology. 2016 Jan;30(1):40-52
Date
Jan-2016
Language
English
Publication Type
Article
Keywords
Adult
Aged
Bipolar Disorder - genetics - psychology
Cognition
Cognition Disorders - genetics - psychology
Endophenotypes
Female
Finland
Gene Expression Profiling
Gene Expression Regulation
Genome-Wide Association Study
Humans
Leukocytes, Mononuclear
Male
Memory
Microarray Analysis
Middle Aged
RNA - analysis
Registries
Schizophrenia - genetics
Schizophrenic Psychology
Sweden
Twins - genetics - psychology
Abstract
We performed a whole-genome expression study to clarify the nature of the biological processes mediating between inherited genetic variations and cognitive dysfunction in schizophrenia.
Gene expression was assayed from peripheral blood mononuclear cells using Illumina Human WG6 v3.0 chips in twins discordant for schizophrenia or bipolar disorder and control twins. After quality control, expression levels of 18,559 genes were screened for association with the California Verbal Learning Test (CVLT) performance, and any memory-related probes were then evaluated for variation by diagnostic status in the discovery sample (N = 190), and in an independent replication sample (N = 73). Heritability of gene expression using the twin design was also assessed.
After Bonferroni correction (p
Notes
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PubMed ID
26710095 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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71 records – page 1 of 8.