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Dopamine Genetic Risk Score Predicts Depressive Symptoms in Healthy Adults and Adults with Depression

 
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Author
Pearson-Fuhrhop, Kristin M.
Dunn, Erin C.HARVARD
Mortero, Sarah
Devan, William J.
Falcone, Guido J.HARVARD
Lee, PhilHARVARD
Holmes, Avram J.HARVARD
Hollinshead, Marisa O.HARVARD
Roffman, Joshua L.HARVARD
Smoller, Jordan W.HARVARD
Rosand, JonathanHARVARD
Cramer, Steven C.
Note: Order does not necessarily reflect citation order of authors.
Published Version
https://doi.org/10.1371/journal.pone.0093772
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Citation
Pearson-Fuhrhop, K. M., E. C. Dunn, S. Mortero, W. J. Devan, G. J. Falcone, P. Lee, A. J. Holmes, et al. 2014. “Dopamine Genetic Risk Score Predicts Depressive Symptoms in Healthy Adults and Adults with Depression.” PLoS ONE 9 (5): e93772. doi:10.1371/journal.pone.0093772. http://dx.doi.org/10.1371/journal.pone.0093772.
Abstract
Background: Depression is a common source of human disability for which etiologic insights remain limited. Although abnormalities of monoamine neurotransmission, including dopamine, are theorized to contribute to the pathophysiology of depression, evidence linking dopamine-related genes to depression has been mixed. The current study sought to address this knowledge-gap by examining whether the combined effect of dopamine polymorphisms was associated with depressive symptomatology in both healthy individuals and individuals with depression. Methods: Data were drawn from three independent samples: (1) a discovery sample of healthy adult participants (n = 273); (2) a replication sample of adults with depression (n = 1,267); and (3) a replication sample of healthy adult participants (n = 382). A genetic risk score was created by combining functional polymorphisms from five genes involved in synaptic dopamine availability (COMT and DAT) and dopamine receptor binding (DRD1, DRD2, DRD3). Results: In the discovery sample, the genetic risk score was associated with depressive symptomatology (β = −0.80, p = 0.003), with lower dopamine genetic risk scores (indicating lower dopaminergic neurotransmission) predicting higher levels of depression. This result was replicated with a similar genetic risk score based on imputed genetic data from adults with depression (β = −0.51, p = 0.04). Results were of similar magnitude and in the expected direction in a cohort of healthy adult participants (β = −0.86, p = 0.15). Conclusions: Sequence variation in multiple genes regulating dopamine neurotransmission may influence depressive symptoms, in a manner that appears to be additive. Further studies are required to confirm the role of genetic variation in dopamine metabolism and depression.
Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4023941/pdf/
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This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page
http://nrs.harvard.edu/urn-3:HUL.InstRepos:12406897

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