Angiotensinogen and angiotensin converting enzyme gene polymorphisms and the risk of bipolar affective disorder in humans

被引:53
作者
Meira-Lima, IV
Pereira, AC
Mota, GFA
Krieger, JE
Vallada, H [1 ]
机构
[1] Univ Sao Paulo, Sch Med, Inst Psychiat, Lab Neurosci LIM 27, Sao Paulo, Brazil
[2] Univ Sao Paulo, Sch Med, Dept Med, Lab Genet & Mol Cardiol LIM 13,Heart Inst InCor, Sao Paulo, Brazil
[3] Univ Fed Sao Paulo, Dept Psychiat, Sao Paulo, Brazil
基金
巴西圣保罗研究基金会;
关键词
affective disorder; renin-angiotensin system; genetic; association study;
D O I
10.1016/S0304-3940(00)01512-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
A possible participation of the renin-angiotensin system (RAS) components with mood disturbances has been suggested in both animal and pharmacological models. In this cross-sectional study, we examined the association between functional polymorphisms in the angiotensin converting enzyme (ACE) and angiotensinogen (AGI) genes in 115 bipolar affective disorder (BPAD) patients and 323 healthy control subjects. The ACE I/D variant did not show any difference in allelic frequencies and genotypic distribution between the groups. in contrast, when studying the AGT M235T polymorphism we found that the M allele was more frequently observed in BPAD patients than in controls (chi (2) = 6.766, d.f. = 1, P = 0.009). Using multivariate logistic models the strongest odds ratio resulted from a dominant genetic model (OR = 3.0; CI (95%) 1.7-5.3] Our data suggest an association between the AGT M235 genotype and increased susceptibility for BPAD in these Brazilian patients. These findings are consistent with the hypothesis that the RAS system plays a role in regulating the mood (C) 2000 Published by Elsevier Science Ireland Ltd.
引用
收藏
页码:103 / 106
页数:4
相关论文
共 25 条
[11]   Distinct mechanism for antidepressant activity by blockade of central substance P receptors [J].
Kramer, MS ;
Cutler, N ;
Feighner, J ;
Shrivastava, R ;
Carman, J ;
Sramek, JJ ;
Reines, SA ;
Liu, GH ;
Snavely, D ;
Wyatt-Knowles, E ;
Hale, JJ ;
Mills, SG ;
MacCoss, M ;
Swain, CJ ;
Harrison, T ;
Hill, RG ;
Hefti, F ;
Scolnick, EM ;
Cascieri, MA ;
Chicchi, GG ;
Sadowski, S ;
Williams, AR ;
Hewson, L ;
Smith, D ;
Carlson, EJ ;
Hargreaves, RJ ;
Rupniak, NMJ .
SCIENCE, 1998, 281 (5383) :1640-1645
[12]   RACIAL ADMIXTURE IN NORTH-EASTERN BRAZIL [J].
KRIEGER, H ;
MORTON, NE ;
MI, MP ;
AZEVEDO, E ;
FREIREMA.A ;
YASUDA, N .
ANNALS OF HUMAN GENETICS, 1965, 29 :113-&
[13]  
MCGUFFIN P, 1994, SEMINARS PSYCHIAT GE, P110
[14]   The ACE deletion polymorphism is not associated with Parkinson's disease [J].
Mellick, GD ;
Buchanan, DD ;
McCann, SJ ;
Davis, DR ;
Le Couteur, DG ;
Chan, D ;
Johnson, AG .
EUROPEAN NEUROLOGY, 1999, 41 (02) :103-106
[15]  
Mervaala E, 1999, J AM SOC NEPHROL, V10, P1669
[16]   Association analyses of the polymorphisms of angiotensin-converting enzyme and angiotensinogen genes with diabetic nephropathy in Japanese non-insulin-dependent diabetics [J].
Ohno, T ;
Kawazu, S ;
Tomono, S .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1996, 45 (02) :218-222
[17]   Reduction of depressive-like behavior in mice lacking angiotensinogen [J].
Okuyama, S ;
Sakagawa, T ;
Sugiyama, F ;
Fukamizu, A ;
Murakami, K .
NEUROSCIENCE LETTERS, 1999, 261 (03) :167-170
[18]   PCR DETECTION OF THE INSERTION DELETION POLYMORPHISM OF THE HUMAN ANGIOTENSIN CONVERTING ENZYME GENE (DCP1) (DIPEPTIDYL CARBOXYPEPTIDASE-1) [J].
RIGAT, B ;
HUBERT, C ;
CORVOL, P ;
SOUBRIER, F .
NUCLEIC ACIDS RESEARCH, 1992, 20 (06) :1433-1433
[19]   A manic depressive history [J].
Risch, N ;
Botstein, D .
NATURE GENETICS, 1996, 12 (04) :351-353
[20]  
Segman RH, 1998, AM J MED GENET, V81, P522