Genome-wide scan for genes involved in bipolar affective disorder in 70 European families ascertained through a bipolar type I early-onset proband: supportive evidence for linkage at 3p14

Preliminary studies suggested that age at onset (AAO) may help to define homogeneous bipolar affective disorder (BPAD) subtypes. This candidate symptom approach might be useful to identify vulnerability genes. Thus, the probability of detecting major disease-causing genes might be increased by focus...

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Published inMolecular psychiatry Vol. 11; no. 7; pp. 685 - 694
Main Authors ETAIN, B, MATHIEU, F, BELLIVIER, F, HENRY, C, DINA, C, GALLINA, S, GURLING, H, MALAFOSSE, A, PREISIG, M, FERRERO, F, CICHON, S, SCHUMACHER, J, RIETSCHEL, M, OHIRAUN, S, BORRMANN-HASSENBACH, M, PROPPING, P, ABOU JAMRA, R, SCHUIZE, T. G, MARUSIC, A, DERNOVSEK, Z. M, GIROS, B, BOURGERON, T, LEMAINQUE, A, MAIER, W, BACQ, D, BETARD, C, CHARON, C, NOTHEN, M. M, LATHROP, M, LEBOYER, M, ALBUS, M, MCKEON, P, ROCHE, S, KEALEY, C, BLACKWOOD, D, MUIR, W
Format Journal Article
LanguageEnglish
Published Basingstoke Nature Publishing Group 01.07.2006
Nature Publishing Group Specialist Journals
Subjects
Adolescent
Adult
Adult and adolescent clinical studies
Age
Age of Onset
Biological and medical sciences
Bipolar Disorder
Bipolar Disorder - classification
Bipolar Disorder - epidemiology
Bipolar Disorder - genetics
Bipolar disorders
Child
Chromosome 3
Chromosome Mapping
Chromosomes
Chromosomes, Human
Chromosomes, Human - genetics
Chromosomes, Human, Pair 3
Chromosomes, Human, Pair 3 - genetics
Europe
Female
Genetic markers
Genetics
Genome, Human
Genomes
Genomic Imprinting
Genomic Imprinting - genetics
Genomics
Hospitals
Human health and pathology
Humans
Kinases
Life Sciences
Linkage analysis
Lod Score
Male
Medical sciences
Microsatellite Repeats
Microsatellites
Mood disorders
Neurosciences
Phenotype
Psychiatrics and mental health
Psychiatry
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Statistics, Nonpar
Statistics, Nonparametric
Europe
Slovenia
United Kingdom > UK
France
Switzerland
Ireland
Germany
Social environment
Human
Mood disorder
Bipolar disorder
linkage
Genetic determinism
Affective disorder
Age of onset
Gene
Family environment
Genetics
Early
genome-wide search
age at onset
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Abstract Preliminary studies suggested that age at onset (AAO) may help to define homogeneous bipolar affective disorder (BPAD) subtypes. This candidate symptom approach might be useful to identify vulnerability genes. Thus, the probability of detecting major disease-causing genes might be increased by focusing on families with early-onset BPAD type I probands. This study was conducted as part of the European Collaborative Study of Early Onset BPAD (France, Germany, Ireland, Scotland, Switzerland, England, Slovenia). We performed a genome-wide search with 384 microsatellite markers using non-parametric linkage analysis in 87 sib-pairs ascertained through an early-onset BPAD type I proband (AAO of 21 years or below). Non-parametric multipoint analysis suggested eight regions of linkage with P-values<0.01 (2p21, 2q14.3, 3p14, 5q33, 7q36, 10q23, 16q23 and 20p12). The 3p14 region showed the most significant linkage (genome-wide P-value estimated over 10 000 simulated replicates of 0.015 [0.01-0.02]). After genome-wide search analysis, we performed additional linkage analyses with increased marker density using markers in four regions suggestive for linkage and having an information contents lower than 75% (3p14, 10q23, 16q23 and 20p12). For these regions, the information content improved by about 10%. In chromosome 3, the non-parametric linkage score increased from 3.51 to 3.83. This study is the first to use early-onset bipolar type I probands in an attempt to increase sample homogeneity. These preliminary findings require confirmation in independent panels of families.
AbstractList Preliminary studies suggested that age at onset (AAO) may help to define homogeneous bipolar affective disorder (BPAD) subtypes. This candidate symptom approach might be useful to identify vulnerability genes. Thus, the probability of detecting major disease-causing genes might be increased by focusing on families with early-onset BPAD type I probands. This study was conducted as part of the European Collaborative Study of Early Onset BPAD (France, Germany, Ireland, Scotland, Switzerland, England, Slovenia). We performed a genome-wide search with 384 microsatellite markers using non-parametric linkage analysis in 87 sib-pairs ascertained through an early-onset BPAD type I proband (AAO of 21 years or below). Non-parametric multipoint analysis suggested eight regions of linkage with P-values<0.01 (2p21, 2q14.3, 3p14, 5q33, 7q36, 10q23, 16q23 and 20p12). The 3p14 region showed the most significant linkage (genome-wide P-value estimated over 10 000 simulated replicates of 0.015 [0.01-0.02]). After genome-wide search analysis, we performed additional linkage analyses with increased marker density using markers in four regions suggestive for linkage and having an information contents lower than 75% (3p14, 10q23, 16q23 and 20p12). For these regions, the information content improved by about 10%. In chromosome 3, the non-parametric linkage score increased from 3.51 to 3.83. This study is the first to use early-onset bipolar type I probands in an attempt to increase sample homogeneity. These preliminary findings require confirmation in independent panels of families.
Preliminary studies suggested that age at onset (AAO) may help to define homogeneous bipolar affective disorder (BPAD) subtypes. This candidate symptom approach might be useful to identify vulnerability genes. Thus, the probability of detecting major disease-causing genes might be increased by focusing on families with early-onset BPAD type I probands. This study was conducted as part of the European Collaborative Study of Early Onset BPAD (France, Germany, Ireland, Scotland, Switzerland, England, Slovenia). We performed a genome-wide search with 384 microsatellite markers using non-parametric linkage analysis in 87 sib-pairs ascertained through an early-onset BPAD type I proband (AAO of 21 years or below). Non-parametric multipoint analysis suggested eight regions of linkage with P-values&lt;0.01 (2p21, 2q14.3, 3p14, 5q33, 7q36, 10q23, 16q23 and 20p12). The 3p14 region showed the most significant linkage (genome-wide P-value estimated over 10 000 simulated replicates of 0.015 [0.01-0.02]). After genome-wide search analysis, we performed additional linkage analyses with increased marker density using markers in four regions suggestive for linkage and having an information contents lower than 75% (3p14, 10q23, 16q23 and 20p12). For these regions, the information content improved by about 10%. In chromosome 3, the non-parametric linkage score increased from 3.51 to 3.83. This study is the first to use early-onset bipolar type I probands in an attempt to increase sample homogeneity. These preliminary findings require confirmation in independent panels of families.
Preliminary studies suggested that age at onset (AAO) may help to define homogeneous bipolar affective disorder (BPAD) subtypes. This candidate symptom approach might be useful to identify vulnerability genes. Thus, the probability of detecting major disease-causing genes might be increased by focusing on families with early-onset BPAD type I probands. This study was conducted as part of the European Collaborative Study of Early Onset BPAD (France, Germany, Ireland, Scotland, Switzerland, England, Slovenia). We performed a genome-wide search with 384 microsatellite markers using non-parametric linkage analysis in 87 sib-pairs ascertained through an early-onset BPAD type I proband (AAO of 21 years or below). Non-parametric multipoint analysis suggested eight regions of linkage with P-values<0.01 (2p21, 2q14.3, 3p14, 5q33, 7q36, 10q23, 16q23 and 20p12). The 3p14 region showed the most significant linkage (genome-wide P-value estimated over 10000 simulated replicates of 0.015 [0.01-0.02]). After genome-wide search analysis, we performed additional linkage analyses with increased marker density using markers in four regions suggestive for linkage and having an information contents lower than 75% (3p14, 10q23, 16q23 and 20p12). For these regions, the information content improved by about 10%. In chromosome 3, the non-parametric linkage score increased from 3.51 to 3.83. This study is the first to use early-onset bipolar type I probands in an attempt to increase sample homogeneity. These preliminary findings require confirmation in independent panels of families.Molecular Psychiatry (2006) 11, 685-694. doi:10.1038/sj.mp.4001815; published online 14 March 2006
Preliminary studies suggested that age at onset (AAO) may help to define homogeneous bipolar affective disorder (BPAD) subtypes. This candidate symptom approach might be useful to identify vulnerability genes. Thus, the probability of detecting major disease-causing genes might be increased by focusing on families with early-onset BPAD type I probands. This study was conducted as part of the European Collaborative Study of Early Onset BPAD (France, Germany, Ireland, Scotland, Switzerland, England, Slovenia). We performed a genome-wide search with 384 microsatellite markers using non parametric linkage analysis in 87 sib-pairs ascertained through an early-onset BPAD type I proband (age at onset of 21 years or below). Non parametric multi-point analysis suggested eight regions of linkage with p-values <0.01 (2p21, 2q14.3, 3p14, 5q33, 7q36, 10q23, 16q23 and 20p12). The 3p14 region showed the most significant linkage (genome-wide p-value estimated over 10.000 simulated replicates of 0.015 [0.01–0.02]). After genome-wide search analysis, we performed additional linkage analyses with increase marker density using markers in four regions suggestive for linkage and having an information contents lower than 75% (3p14, 10q23, 16q23 and 20p12). For these regions, the information content improved by about 10%. In chromosome 3, the non parametric linkage score increased from 3.51 to 3.83. This study is the first to use early onset bipolar type I probands in an attempt to increase sample homogeneity. These preliminary findings require confirmation in independent panels of families.
Audience Academic
Author BETARD, C
FERRERO, F
SCHUIZE, T. G
LEMAINQUE, A
MUIR, W
ETAIN, B
ROCHE, S
PROPPING, P
BOURGERON, T
CICHON, S
PREISIG, M
GALLINA, S
LATHROP, M
MARUSIC, A
BACQ, D
OHIRAUN, S
NOTHEN, M. M
ALBUS, M
MCKEON, P
MATHIEU, F
CHARON, C
BELLIVIER, F
RIETSCHEL, M
KEALEY, C
MAIER, W
SCHUMACHER, J
LEBOYER, M
DINA, C
GURLING, H
BORRMANN-HASSENBACH, M
ABOU JAMRA, R
DERNOVSEK, Z. M
MALAFOSSE, A
BLACKWOOD, D
GIROS, B
HENRY, C
AuthorAffiliation 20 CNG Centre National de Génotypage 91030 Evry,FR
7 Smurfit Institute of Genetics Trinity College Dublin 2,IE
8 Department of Pharmacology University of Pennsylvania Philadelphia,US
12 Molecular Psychiatry Laboratory - Department of Psychiatry and Behavioural Sciences Windeyer Institute for Medical Sciences Royal Free and University College London Medical School London,GB
1 Neurobiologie et Psychiatrie INSERM : U513 Université Paris XII Val de Marne 8, Rue du Général Sarrail 94010 CRETEIL,FR
16 Life & Brain Center - Department of Genomics University of Bonn Bonn,DE
3 Division of Genetic Epidemiology in Psychiatry Central Institute of Mental Health Mannheim,DE
11 Génétique des maladies multifactorielles CNRS : UMR8090 Université du Droit et de la Santé - Lille II 1 Rue du professeur Calmette, 59019 LILLE,FR
2 Département de psychiatrie Hôpital Albert Chenevier Hôpital Henri Mondor AP-HP 94000 Créteil,FR
9 Division of Psychiatry Royal Edinburgh Hospital University of Edinburgh Edinburgh,GB
19 Gén
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Issue 7
Keywords Social environment
Human
Mood disorder
Bipolar disorder
linkage
Genetic determinism
Affective disorder
Age of onset
Gene
Family environment
Genetics
Early
genome-wide search
age at onset
Language English
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SSID ssj0014765
Score 2.1580377
Snippet Preliminary studies suggested that age at onset (AAO) may help to define homogeneous bipolar affective disorder (BPAD) subtypes. This candidate symptom...
SourceID pubmedcentral
hal
proquest
gale
crossref
pubmed
pascalfrancis
nature
SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage 685
SubjectTerms Adolescent
Adult
Adult and adolescent clinical studies
Age
Age of Onset
Biological and medical sciences
Bipolar Disorder
Bipolar Disorder - classification
Bipolar Disorder - epidemiology
Bipolar Disorder - genetics
Bipolar disorders
Child
Chromosome 3
Chromosome Mapping
Chromosomes
Chromosomes, Human
Chromosomes, Human - genetics
Chromosomes, Human, Pair 3
Chromosomes, Human, Pair 3 - genetics
Europe
Female
Genetic markers
Genetics
Genome, Human
Genomes
Genomic Imprinting
Genomic Imprinting - genetics
Genomics
Hospitals
Human health and pathology
Humans
Kinases
Life Sciences
Linkage analysis
Lod Score
Male
Medical sciences
Microsatellite Repeats
Microsatellites
Mood disorders
Neurosciences
Phenotype
Psychiatrics and mental health
Psychiatry
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Statistics, Nonpar
Statistics, Nonparametric
Title Genome-wide scan for genes involved in bipolar affective disorder in 70 European families ascertained through a bipolar type I early-onset proband: supportive evidence for linkage at 3p14
URI http://dx.doi.org/10.1038/sj.mp.4001815
https://www.ncbi.nlm.nih.gov/pubmed/16534504
https://www.proquest.com/docview/221233461
https://www.proquest.com/docview/2645751315
https://search.proquest.com/docview/68580312
https://search.proquest.com/docview/759316445
https://inserm.hal.science/inserm-00132874
https://pubmed.ncbi.nlm.nih.gov/PMC1959341
Volume 11
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