Significant linkage to chromosome 22q for exploratory eye movement dysfunction in schizophrenia

被引:39
作者
Takahashi, S
Ohtsuki, T
Yu, SY
Tanabe, E
Yara, K
Kamioka, M
Matsushima, E
Matsuura, M
Ishikawa, K
Minowa, Y
Noguchi, E
Nakayama, J
Yamakawa-Kobayashi, K
Arinami, T [1 ]
Kojima, T
机构
[1] Univ Tsukuba, Inst Basic Med Sci, Dept Med Genet, Tsukuba, Ibaraki 3058575, Japan
[2] Nihon Univ, Sch Med, Dept Neuropsychiat, Tokyo, Japan
[3] Tokyo Med & Dent Univ, Fac Med, Dept Neuropsychiat, Tokyo 113, Japan
[4] Nihon Univ, Sch Med, Dept Pharmacol, Tokyo, Japan
关键词
endophenotype; schizophrenia; eye movement; linkage; quantitative trait locus; nonparametric;
D O I
10.1002/ajmg.b.10046
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
A genome-wide scan for a locus responsible for exploratory eye movement (EEM), which is quantitative and can be disturbed in association with schizophrenia, was performed. A 10-cM resolution genome-wide linkage analysis of the EEM disturbance with 358 highly polymorphic microsatellite markers in 38 nuclear families with 122 members (38 probands, 47 sibs, and 37 parents) including 58 sib-pairs yielded the suggestive linkage to the GCT10C10 marker on chromosome 22q11.2 (LOD=2.48). Dense mapping with additional markers around the GCT10C10 marker yielded evidence for significant linkage between EEM disturbance and markers D22S429 and D22S310 on chromosome 22q12.1 (LOD score of 4.63) with suggestive evidence for the chromosome region 22q11.2-q12.1. Our findings suggest that a relatively small number of loci may control the schizophrenia-related quantitative EEM trait. We believe that identifying gene(s) on chromosome 22q associated with the EEM phenotype may forward our understanding of the etiology of schizophrenia. (C) 2003 Wiley-Liss, Inc.
引用
收藏
页码:27 / 32
页数:6
相关论文
共 46 条
[1]  
Arolt V, 1996, AM J MED GENET, V67, P564, DOI 10.1002/(SICI)1096-8628(19961122)67:6<564::AID-AJMG10>3.0.CO
[2]  
2-R
[3]  
Arolt V, 1999, AM J MED GENET, V88, P603, DOI 10.1002/(SICI)1096-8628(19991215)88:6<603::AID-AJMG5>3.3.CO
[4]  
2-O
[5]   Schizophrenia susceptibility loci on chromosomes 13q32 and 8p21 [J].
Blouin, JL ;
Dombroski, BA ;
Nath, SK ;
Lasseter, VK ;
Wolyniec, PS ;
Nestadt, G ;
Thornquist, M ;
Ullrich, G ;
McGrath, J ;
Kasch, L ;
Lamacz, M ;
Thomas, MG ;
Gehrig, C ;
Radhakrishna, U ;
Snyder, SE ;
Balk, KG ;
Neufeld, K ;
Swartz, KL ;
DeMarchi, N ;
Papadimitriou, GN ;
Dikeos, DG ;
Stefanis, CN ;
Chakravarti, A ;
Childs, B ;
Housman, DE ;
Kazazian, HH ;
Antonarakis, SE ;
Pulver, AE .
NATURE GENETICS, 1998, 20 (01) :70-73
[6]  
Calkins ME, 2000, AM J MED GENET, V97, P72, DOI 10.1002/(SICI)1096-8628(200021)97:1<72::AID-AJMG10>3.0.CO
[7]  
2-L
[8]   Psychophysiological measures of (dis)inhibition as liability indicators for schizophrenia [J].
Clementz, BA .
PSYCHOPHYSIOLOGY, 1998, 35 (06) :648-668
[9]   ANALYSIS OF CHROMOSOME-22 MARKERS IN 9 SCHIZOPHRENIA PEDIGREES [J].
COON, H ;
HOLIK, J ;
HOFF, M ;
REIMHERR, F ;
WENDER, P ;
MYLESWORSLEY, M ;
WALDO, M ;
FREEDMAN, R ;
BYERLEY, W .
AMERICAN JOURNAL OF MEDICAL GENETICS, 1994, 54 (01) :72-79
[10]   Alternative phenotypes for the complex genetics of schizophrenia [J].
Freedman, R ;
Adler, LE ;
Leonard, S .
BIOLOGICAL PSYCHIATRY, 1999, 45 (05) :551-558