University of Worcester Worcester Research and Publications
 
  USER PANEL:
  ABOUT THE COLLECTION:
  CONTACT DETAILS:

Phenotypic Association Analyses with Copy Number Variation in Recurrent Depressive Disorder

Rucker, J.J.H. and Tansey, K.E. and Rivera, M. and Pinto, D. and Cohen-Woods, S. and Uher, R. and Aitchison, K.J. and Craddock, N. and Owen, M.J. and Jones, Lisa and Jones, I. and Korszun, A. and Barnes, M.R. and Preisig, M. and Mors, O. and Maier, W. and Rice, J. and Rietschel, M. and Holsboer, F. and Farmer, A.E. and Craig, I.W. and Scherer, S.W. and McGuffin, P. and Breen, G. (2016) Phenotypic Association Analyses with Copy Number Variation in Recurrent Depressive Disorder. Biological Psychiatry, 79 (4). pp. 329-336. ISSN Online: 0006-3223

Full text not available from this repository. (Request a copy)

Abstract

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.

Item Type: Article
Additional Information:

The full-text can be accessed via the official URL.
Open Access funded by Wellcome Trust.

Uncontrolled Keywords: affective disorders, copy number variation, depression, genetics, phenotypes
Subjects: B Philosophy. Psychology. Religion > BF Psychology
R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Divisions: Academic Departments > Institute of Health and Society
Related URLs:
Copyright Info: Open Access article
Depositing User: Lisa Jones
Date Deposited: 30 Oct 2015 09:05
Last Modified: 22 Apr 2016 16:28
URI: https://eprints.worc.ac.uk/id/eprint/4023

Actions (login required)

View Item View Item
 
     
Worcester Research and Publications is powered by EPrints 3 which is developed by the School of Electronics and Computer Science at the University of Southampton. More information and software credits.