Get 20M+ Full-Text Papers For Less Than $1.50/day. Subscribe now for You or Your Team.

Learn More →

Combined action of the ACE D- and the G-protein β3 T-allele in major depression: a possible link to cardiovascular disease?

Combined action of the ACE D- and the G-protein β3 T-allele in major depression: a possible link... 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 β3-subunit (Gβ3) 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 Gβ3 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 (χ2 = 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 Gβ3 genotypes accumulate in carriers of the ACE D allele (ID and DD) and Gβ3 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–Gβ3 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular Psychiatry Springer Journals

Combined action of the ACE D- and the G-protein β3 T-allele in major depression: a possible link to cardiovascular disease?

Loading next page...
 
/lp/springer-journals/combined-action-of-the-ace-d-and-the-g-protein-3-t-allele-in-major-GSSmzj5F0Q

References (50)

Publisher
Springer Journals
Copyright
Copyright © 2002 by Macmillan Publishers Limited
Subject
Medicine & Public Health; Medicine/Public Health, general; Psychiatry; Neurosciences; Behavioral Sciences; Pharmacotherapy; Biological Psychology
ISSN
1359-4184
eISSN
1476-5578
DOI
10.1038/sj.mp.4001149
Publisher site
See Article on Publisher Site

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 β3-subunit (Gβ3) 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 Gβ3 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 (χ2 = 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 Gβ3 genotypes accumulate in carriers of the ACE D allele (ID and DD) and Gβ3 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–Gβ3 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.

Journal

Molecular PsychiatrySpringer Journals

Published: Dec 12, 2002

There are no references for this article.