Phenotypic Association Analyses With Copy Number Variation in Recurrent Depressive Disorder.

Détails

Ressource 1Télécharger: BIB_32355C8454B3.P001.pdf (177.82 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_32355C8454B3
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Phenotypic Association Analyses With Copy Number Variation in Recurrent Depressive Disorder.
Périodique
Biological Psychiatry
Auteur(s)
Rucker J.J., Tansey K.E., Rivera M., Pinto D., Cohen-Woods S., Uher R., Aitchison K.J., Craddock N., Owen M.J., Jones L., Jones I., Korszun A., Barnes M.R., Preisig M., Mors O., Maier W., Rice J., Rietschel M., Holsboer F., Farmer A.E., Craig I.W., Scherer S.W., McGuffin P., Breen G.
ISSN
1873-2402 (Electronic)
ISSN-L
0006-3223
Statut éditorial
Publié
Date de publication
2016
Peer-reviewed
Oui
Volume
79
Numéro
4
Pages
329-336
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
BACKGROUND: Defining the molecular genomic basis of the likelihood of developing depressive disorder is a considerable challenge. We previously associated rare, exonic deletion copy number variants (CNV) with recurrent depressive disorder (RDD). Sex chromosome abnormalities also have been observed to co-occur with RDD.
METHODS: In this reanalysis of our RDD dataset (N = 3106 cases; 459 screened control samples and 2699 population control samples), we further investigated the role of larger CNVs and chromosomal abnormalities in RDD and performed association analyses with clinical data derived from this dataset.
RESULTS: We found an enrichment of Turner's syndrome among cases of depression compared with the frequency observed in a large population sample (N = 34,910) of live-born infants collected in Denmark (two-sided p = .023, odds ratio = 7.76 [95% confidence interval = 1.79-33.6]), a case of diploid/triploid mosaicism, and several cases of uniparental isodisomy. In contrast to our previous analysis, large deletion CNVs were no more frequent in cases than control samples, although deletion CNVs in cases contained more genes than control samples (two-sided p = .0002).
CONCLUSIONS: After statistical correction for multiple comparisons, our data do not support a substantial role for CNVs in RDD, although (as has been observed in similar samples) occasional cases may harbor large variants with etiological significance. Genetic pleiotropy and sample heterogeneity suggest that very large sample sizes are required to study conclusively the role of genetic variation in mood disorders.
Mots-clé
Adolescent, Adult, Case-Control Studies, Chromosome Aberrations/statistics & numerical data, DNA Copy Number Variations/genetics, Databases, Genetic, Depressive Disorder/genetics, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Linear Models, Male, Middle Aged, Young Adult
Pubmed
Web of science
Open Access
Oui
Création de la notice
16/04/2015 9:56
Dernière modification de la notice
20/08/2019 14:17
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