ArticleMolecular psychiatry2002
Combined action of the ACE D- and the G-protein beta3 T-allele in major depression: a possible link to cardiovascular disease?
Article in Molecular psychiatry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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20 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Meta-analyses of genetic studies on major depressive disorder.Molecular psychiatry · 2008Pooled it
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- Genetic Analysis ofInternational journal of medical sciences · 2016Article
- Depressed mood and cause-specific mortality: a 40-year general community assessment.Annals of epidemiology · 2012Article
- Association of somatic and cognitive depressive symptoms and biomarkers in acute myocardial infarction: insights from the translational research investigating underlying disparities in acute myocardial infarction patients' health status registry.Biological psychiatry · 2012Article
- Depressive subtype a predictor of cardiovascular morbidity.Current psychiatry reports · 2008Article
- The interdependence of behavioral and somatic health: implications for conceptualizing health and measuring treatment outcomes.International journal of integrated care · 2007Article
- Interaction between TPH1 and GNB3 genotypes and electroconvulsive therapy in major depression.Journal of neural transmission (Vienna, Austria : 1996) · 2007Article
- Common genetic factors for depression and cardiovascular disease.Dialogues in clinical neuroscience · 2007Review
- Association between a functional polymorphism in the renin-angiotensin system and completed suicide.Journal of neural transmission (Vienna, Austria : 1996) · 2006Article
- [The value of pharmacogenetic tests in antidepressive medication therapy].Der Nervenarzt · 2005Review
- Candidate genes for antidepressant response to selective serotonin reuptake inhibitors.Neuropsychiatric disease and treatment · 2005Article
- Pharmacogenomics in depression and antidepressants.Dialogues in clinical neuroscience · 2005Review
- Pharmacogenetics of antidepressants and antipsychotics: the contribution of allelic variations to the phenotype of drug response.Molecular psychiatry · 2004Review
- Pharmacogenetics and psychiatry.Current psychiatry reports · 2004Review
- Association between a G-protein beta 3 subunit gene polymorphism and the symptomatology and treatment responses of major depressive disorders.The pharmacogenomics journal · 2004Article
- Common genetic risk factors for psychiatric and simatic disorders.Dialogues in clinical neuroscience · 2003Article
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10 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Although it is well established that depression is a major risk factor for the development of coronary artery disease and that cerebrovascular disease can be a major contributing factor for the development of depression, the information about the interplay between the central nervous system and cardiovascular disease is still limited. We investigated the angiotensin I converting enzyme (ACE) ID and the G-protein beta3-subunit (Gbeta3) C825T polymorphism in 201 patients with unipolar major depression and 161 ethnically and age-matched controls. Both gene variants have earlier been associated with either cardiovascular disease or affective disorders, making them good candidates for a combined analysis. We found a significant increase in the Gbeta3 T allele (OR = 1.61, 95% CI 1.17-2.2, P = 0.0035) and a marginal altered genotype distribution of the ACE ID polymorphism with decrease in the II genotypes (chi(2) = 6.43, df=3, P = 0.04) in the patients' group. Analysing the data for both genes we found that the combined actions of ACE and Gbeta3 genotypes accumulate in carriers of the ACE D allele (ID and DD) and Gbeta3 TT homozygotes with ID/DD-TT carriers showing a more than five-fold increase in risk for major depression (crude OR = 5.83, 95% CI 1.99-17.08, P = 0.0002). As our study was carried out with depressive patients without serious cardiac impairment at the time of the investigation, we are presently unable to predict whether this combined action of the ACE ID/DD-Gbeta3 TT genotype is increasing the risk for both disorders. Nevertheless our study reports for the first time that the same allelic combination of two genes that have been shown to increase the risk for myocardial infarction (Naber et al, 2000) increase the vulnerability for depressive disorder.
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