ORIGINAL ARTICLESAngiotensinogen M235T polymorphism and symptoms of depression in a population-based study and a family-based studyLópez-León, Sandraa; J.W. Janssens, A. Cecileb; Tiemeier, Henninga; Hofman, Alberta; Aulchenko, Yurii S.a; Snijders, Pieter J.L.M.a; Claes, Stephand e; Oostra, Ben A.c; van Duijn, Cornelia M.aAuthor Information Departments of aEpidemiology and Biostatistics bPublic Health cClinical Genetics, Erasmus University Medical Center, Rotterdam, The Netherlands dMolecular Genetics Department, Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Antwerp eCenter for Human Genetics, University of Leuven, Leuven, Belgium Correspondence to Dr Cornelia M. van Duijn, PhD, Professor, Department of Epidemiology and Biostatistics, Erasmus MC University Medical Center Rotterdam, PO Box 2040, 3000 CA Rotterdam, The Netherlands Tel: +31 10 7043394; fax: +31 10 7044657; e-mail: [email protected] Received 10 January 2007 Accepted 26 September 2007 Psychiatric Genetics: August 2008 - Volume 18 - Issue 4 - p 162-166 doi: 10.1097/YPG.0b013e3282fb7fd6 Buy Metrics Abstract Background Evidence suggests that the angiotensinogen (AGT) gene is involved in depression. The aim of this paper is to examine the association between the AGT M235T polymorphism and symptoms of depression in two independent populations; a population-based study, and a family-based study. Methods Symptoms of depression were scored using the Centre of Epidemiological Studies Depression Scale (CES-D) and compared between the MM, MT, and TT genotype groups. The extent to which AGT M235T explains the heritability of the scores was examined using a variance components analysis. Results A significant relationship between the AGT M235T polymorphism and CES-D scores was found in men in both populations. The heritability estimate was 32%. The AGT genotype contributed to 1% of the total variance of the CES-D scores. Conclusion Our findings suggest that the AGT gene is involved in the aetiology of symptoms of depression in men. © 2008 Lippincott Williams & Wilkins, Inc.