Shared genetic etiology between alcohol dependence and major depressive disorder. Foo, J. C., Streit, F., Treutlein, J., Ripke, S., Witt, S. H., Strohmaier, J., Degenhardt, F., Forstner, A. J., Hoffmann, P., Soyka, M., Dahmen, N., Scherbaum, N., Wodarz, N., Heilmann-Heimbach, S., Herms, S., Cichon, S., Preuss, U., Gaebel, W., Ridinger, M., Hoffmann, S., Schulze, T. G., Maier, W., Zill, P., Müller-Myhsok, B., Ising, M., Lucae, S., Nöthen, M. M., Mann, K., Kiefer, F., Rietschel, M., Frank, J., & Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium Psychiatric Genetics, 28(4):66–70, 2018.
doi  abstract   bibtex   
The clinical comorbidity of alcohol dependence (AD) and major depressive disorder (MDD) is well established, whereas genetic factors influencing co-occurrence remain unclear. A recent study using polygenic risk scores (PRS) calculated based on the first-wave Psychiatric Genomics Consortium MDD meta-analysis (PGC-MDD1) suggests a modest shared genetic contribution to MDD and AD. Using a (∼10 fold) larger discovery sample, we calculated PRS based on the second wave (PGC-MDD2) of results, in a severe AD case-control target sample. We found significant associations between AD disease status and MDD-PRS derived from both PGC-MDD2 (most informative P-threshold=1.0, P=0.00063, R=0.533%) and PGC-MDD1 (P-threshold=0.2, P=0.00014, R=0.663%) meta-analyses; the larger discovery sample did not yield additional predictive power. In contrast, calculating PRS in a MDD target sample yielded increased power when using PGC-MDD2 (P-threshold=1.0, P=0.000038, R=1.34%) versus PGC-MDD1 (P-threshold=1.0, P=0.0013, R=0.81%). Furthermore, when calculating PGC-MDD2 PRS in a subsample of patients with AD recruited explicitly excluding comorbid MDD, significant associations were still found (n=331; P-threshold=1.0, P=0.042, R=0.398%). Meanwhile, in the subset of patients in which MDD was not the explicit exclusion criteria, PRS predicted more variance (n=999; P-threshold=1.0, P=0.0003, R=0.693%). Our findings replicate the reported genetic overlap between AD and MDD and also suggest the need for improved, rigorous phenotyping to identify true shared cross-disorder genetic factors. Larger target samples are needed to reduce noise and take advantage of increasing discovery sample size.
@article{foo_shared_2018,
	title = {Shared genetic etiology between alcohol dependence and major depressive disorder},
	volume = {28},
	issn = {1473-5873},
	doi = {10.1097/YPG.0000000000000201},
	abstract = {The clinical comorbidity of alcohol dependence (AD) and major depressive disorder (MDD) is well established, whereas genetic factors influencing co-occurrence remain unclear. A recent study using polygenic risk scores (PRS) calculated based on the first-wave Psychiatric Genomics Consortium MDD meta-analysis (PGC-MDD1) suggests a modest shared genetic contribution to MDD and AD. Using a (∼10 fold) larger discovery sample, we calculated PRS based on the second wave (PGC-MDD2) of results, in a severe AD case-control target sample. We found significant associations between AD disease status and MDD-PRS derived from both PGC-MDD2 (most informative P-threshold=1.0, P=0.00063, R=0.533\%) and PGC-MDD1 (P-threshold=0.2, P=0.00014, R=0.663\%) meta-analyses; the larger discovery sample did not yield additional predictive power. In contrast, calculating PRS in a MDD target sample yielded increased power when using PGC-MDD2 (P-threshold=1.0, P=0.000038, R=1.34\%) versus PGC-MDD1 (P-threshold=1.0, P=0.0013, R=0.81\%). Furthermore, when calculating PGC-MDD2 PRS in a subsample of patients with AD recruited explicitly excluding comorbid MDD, significant associations were still found (n=331; P-threshold=1.0, P=0.042, R=0.398\%). Meanwhile, in the subset of patients in which MDD was not the explicit exclusion criteria, PRS predicted more variance (n=999; P-threshold=1.0, P=0.0003, R=0.693\%). Our findings replicate the reported genetic overlap between AD and MDD and also suggest the need for improved, rigorous phenotyping to identify true shared cross-disorder genetic factors. Larger target samples are needed to reduce noise and take advantage of increasing discovery sample size.},
	language = {eng},
	number = {4},
	journal = {Psychiatric Genetics},
	author = {Foo, Jerome C. and Streit, Fabian and Treutlein, Jens and Ripke, Stephan and Witt, Stephanie H. and Strohmaier, Jana and Degenhardt, Franziska and Forstner, Andreas J. and Hoffmann, Per and Soyka, Michael and Dahmen, Norbert and Scherbaum, Norbert and Wodarz, Norbert and Heilmann-Heimbach, Stefanie and Herms, Stefan and Cichon, Sven and Preuss, Ulrich and Gaebel, Wolfgang and Ridinger, Monika and Hoffmann, Sabine and Schulze, Thomas G. and Maier, Wolfgang and Zill, Peter and Müller-Myhsok, Bertram and Ising, Marcus and Lucae, Susanne and Nöthen, Markus M. and Mann, Karl and Kiefer, Falk and Rietschel, Marcella and Frank, Josef and {Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium}},
	year = {2018},
	pmid = {29901528},
	pmcid = {PMC6039372},
	pages = {66--70},
}
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