Evaluation of the genes for the adrenergic receptors α2A and α1C and Gilles de la Tourette syndrome

被引:10
作者
Xu, C
Ozbay, F
Wigg, K
Shulman, R
Tahir, E
Yazgan, Y
Sandor, P
Barr, CL
机构
[1] Toronto Western Hosp, Dept Psychiat, Div Cellular & Mol Biol, Toronto, ON M5T 2S8, Canada
[2] Marmara Univ Med Sch, Dev & Neuropsychiat Unit, Istanbul, Turkey
[3] Inst Psychiat, London, England
[4] Univ Toronto, Dept Psychiat, Toronto, ON, Canada
[5] Hosp Sick Children, Dept Psychiat, Toronto, ON M5G 1X8, Canada
来源
AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS | 2003年 / 119B卷 / 01期
关键词
Gilles de la Tourette syndrome; genetics; adrenergic receptor alpha 1C (alpha la); adrenergic receptor alpha 2A; linkage;
D O I
10.1002/ajmg.b.20001
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Gilles de la Tourette Syndrome (GTS) has long been known to be familial, and evidence from twin studies indicates that it has a substantial genetic component. Our genome scan of sibling pair families with GTS found evidence suggestive of linkage to several chromosomal locations. On the basis of these findings, we have begun to study additional markers in these regions, with some of the markers located in candidate genes. Two candidate genes stand out in these regions: the adrenergic receptor alpha1C(1A) (ADRA1C) located on chromosome 8p and the adrenergic receptor alpha2A (ADRA2A) located on chromosome 10q. The adrenergic system has been suggested to play a role in GTS based on the reduction of symptoms with the adrenergic receptor agonists, clonidine and guanfacine. We examined the inheritance of polymorphisms in the ADRA2A and ADRA1C genes in 113 nuclear families identified through a GTS proband. We found no significant evidence for linkage using the transmission disequilibrium test for these two genes. Based on our families, we conclude that these genes are not major genetic factors contributing to the susceptibility to GTS. (C) 2003 Wiley-Liss, Inc.
引用
收藏
页码:54 / 59
页数:6
相关论文
共 31 条
  • [1] Arnsten AFT, 1996, ARCH GEN PSYCHIAT, V53, P448
  • [2] Barr CL, 1999, AM J MED GENET, V88, P437, DOI 10.1002/(SICI)1096-8628(19990820)88:4<437::AID-AJMG24>3.0.CO
  • [3] 2-E
  • [4] Attention-deficit hyperactivity disorder and the adrenergic receptors α1C and α2C
    Barr, CL
    Wigg, K
    Zai, G
    Roberts, W
    Malone, M
    Schachar, R
    Tannock, R
    Kennedy, JL
    [J]. MOLECULAR PSYCHIATRY, 2001, 6 (03) : 334 - 337
  • [5] Barrow TD, 1998, GEOTIMES, V43, P4
  • [6] CHAMBERS WJ, 1985, ARCH GEN PSYCHIAT, V42, P696
  • [7] GUANFACINE TREATMENT OF COMORBID ATTENTION-DEFICIT HYPERACTIVITY DISORDER AND TOURETTES-SYNDROME - PRELIMINARY CLINICAL-EXPERIENCE
    CHAPPELL, PB
    RIDDLE, MA
    SCAHILL, L
    LYNCH, KA
    SCHULTZ, R
    ARNSTEN, A
    LECKMAN, JF
    COHEN, DJ
    [J]. JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY, 1995, 34 (09) : 1140 - 1146
  • [8] Human immunodeficiency virus infection and genital ulcer disease in South Africa -: The herpetic connection
    Chen, CY
    Ballard, RC
    Beck-Sague, CM
    Dangor, Y
    Radebe, F
    Schmid, S
    Weiss, JB
    Tshabalala, V
    Fehler, G
    Htun, Y
    Morse, SA
    [J]. SEXUALLY TRANSMITTED DISEASES, 2000, 27 (01) : 21 - 29
  • [9] Additive effect of three noradrenergic genes (ADRA2A, ADRA2C, DBH) on attention-deficit hyperactivity disorder and learning disabilities in Tourette syndrome subjects
    Comings, DE
    Gade-Andavolu, R
    Gonzalez, N
    Blake, H
    Wu, SJ
    MacMurray, JP
    [J]. CLINICAL GENETICS, 1999, 55 (03) : 160 - 172
  • [10] Subtypes of functional α1- and α2-adrenoceptors
    Docherty, JR
    [J]. EUROPEAN JOURNAL OF PHARMACOLOGY, 1998, 361 (01) : 1 - 15