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Is there a common genetic link for depression and cardiovascular disease?

A large body of evidence has emerged over several years for an association between depressive disorder and cardiovascular disease. Although many studies have shown that depression increases the risk for coronary artery disease and the mortality rates after myocardial infarction, there is recent support for the assumption that the relation between both disorders may be bi-directional. The mechanisms of this interaction are at present uncertain and several factors, including stress with its multiple actions on brain and peripheral organs, acute inflammatory reactions with altered immune function as well as a genetically driven susceptibility to develop the disorders are under debate.

Regarding the genetic contribution, variants in two genes were repeatedly discussed as important predisposing factor for cardiovascular function and disease. The gene coding for the angiotensin-converting-enzyme (ACE), an enzyme which is involved in the development of hypertension and other cardiovascular distress, has a common mutation (allele-D) which results in increased ACE concentration (consequently, ACE inhibitors are used as antihypertensive agents). Several studies have shown an association between this allele-D and cardiovascular disorders, supporting the hypothesis of a genetic contribution. However, not only the actual concentration of ACE but also other factors are relevant for cardiovascular function and the development of diseases. Among those is the transduction of nervous signals, which is regulated by various components, including G-proteins. G-proteins are located within the cellular membranes and are thus key elements for the signal transduction, as they induce a cascade of cell reactions after the incoming signal. Thus alterations in the function of these G-proteins could have tremendous effects upon rapidity and quality of the nervous signal transmission. And recently a mutation in one subtype of these G-protein genes, the G-3 subunit allele-T was observed n
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Contact: Aimee Midei
molecularpsychiatry@mednet.ucla.edu
310-206-6739
Molecular Psychiatry
9-Dec-2002


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