No association between bipolar disorder and alleles at a functional polymorphism in the COMT gene - Biomed European Bipolar Collaborative Group

被引:45
作者
Craddock, N
Spurlock, G
McGuffin, P
Owen, MJ
NostenBertrand, M
Bellivier, F
Meloni, R
Leboyer, M
Mallet, J
MynettJohnson, L
Murphy, V
McKeon, P
Kirov, G
Powell, J
Kunugi, H
Collier, D
Larosa, M
Nacmias, B
Sorbi, S
Schwab, S
Ackenheil, M
Maier, W
机构
[1] HOP LA PITIE SALPETRIERE, CNRS, LGN, PARIS, FRANCE
[2] ST PATRICKS HOSP, DUBLIN, IRELAND
[3] INST PSYCHIAT, LONDON, ENGLAND
[4] UNIV FLORENCE, DEPT NEUROL & PSYCHIAT SCI, FLORENCE, ITALY
[5] UNIV MUNICH, NEVERENKLIN, MUNICH, GERMANY
[6] UNIV BONN, DEPT PSYCHIAT, D-5300 BONN, GERMANY
关键词
D O I
10.1192/bjp.170.6.526
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Background There is compelling evidence For the existence of susceptibility genes for bipolar disorder. Association studies using functional DNA variations are an important approach for identifying these genes. The enzyme catechol-O-methyltransferase (COMT) plays a key role in the degradation of catecholamine neurotransmitters and is a candidate For involvement in bipolar disorder. Recently a common functional genetic polymorphism that underlies population variation in COMT activity has been elucidated and a simple assay developed. Method In a collaboration involving seven European centres, we have undertaken an association study of this Functional polymorphism in 412 unrelated West European caucasian DSM - III - R bipolar patients and 368 ethnically matched controls. Results We found no evidence of allelic or genotypic association. Conclusions We can conclude that variation at this functional polymorphism does not make an important contribution to bipolar disorder in the Western European population. Future studies using this powerful experimental approach can be expected to contribute to identification of bipolar susceptibility genes.
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页码:526 / 528
页数:3
相关论文
共 17 条
  • [1] The efficacy of 2 different dosages of methylphenidate in treating adults with attention-deficit hyperactivity disorder
    Bouffard, R
    Hechtman, L
    Minde, K
    Iaboni-Kassab, F
    [J]. CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE, 2003, 48 (08): : 546 - 554
  • [2] Cohen J., 1988, Statistical Power Analysis for the Behavioral Sciences, V2
  • [3] CRADDOCK N, 1995, AM J HUM GENET, V57, P690
  • [4] Psychiatric genetics
    Craddock, N
    [J]. BRITISH JOURNAL OF PSYCHIATRY, 1996, 169 (03) : 386 - 392
  • [5] ENDICOTT J, 1978, ARCH GEN PSYCHIAT, V35, P837
  • [6] GERSHON ES, 1975, ARCH GEN PSYCHIAT, V32, P1351
  • [7] GERSHON ES, 1980, ENZYMES NEUROTRANSMI, P281
  • [8] Goodwin F.K., 2007, MANIC DEPRESSIVE ILL
  • [9] CHROMOSOMAL MAPPING OF THE HUMAN CATECHOL-O-METHYLTRANSFERASE GENE TO 22Q11.1-]Q11.2
    GROSSMAN, MH
    EMANUEL, BS
    BUDARF, ML
    [J]. GENOMICS, 1992, 12 (04) : 822 - 825
  • [10] KUNUGI H, 1997, IN PRESS BIOL PSYCHI