CNR1, central cannabinoid receptor gene, associated with susceptibility to hebephrenic schizophrenia

被引:173
作者
Ujike, H
Takaki, M
Nakata, K
Tanaka, Y
Takeda, T
Kodama, M
Fujiwara, Y
Sakai, A
Kuroda, S
机构
[1] Okayama Univ, Grad Sch Med & Dent, Dept Neuropsychiat, Okayama 7008558, Japan
[2] Zikei Hosp, Okayama, Japan
[3] Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD USA
[4] Takami Hosp, Okayama, Japan
[5] Takaoka Hosp, Himeji, Hyogo, Japan
[6] Kasaoka Hosp, Honshu, Japan
关键词
CNR1; gene; cannabinoid receptor; schizophrenia; hebephrenic type; Japanese; association study;
D O I
10.1038/sj.mp.4001029
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
To examine the cannabinoid hypothesis for pathogenesis of schizophrenia, we examined two kinds of polymorphisms of the CNR1 gene, which encodes human CB1 receptor, a subclass of central cannabinoid receptors, in schizophrenics and age-matched controls in the Japanese population. Allelic and genotypic distributions of polymorphism 1359G/A at codon 453 in the coding region and AAT triplet repeats in the 3' flanking region in the Japanese population were quite different from those in Caucasians. Although the polymorphism 1359G/A was not associated with schizophrenia, the triplet repeat polymorphism of the CNR1 gene was significantly associated with schizophrenia, especially the hebephrenic subtype (P = 0.0028). Hebephrenic schizophrenia showed significantly increased rate of the 9 repeat allele (P = 0.032, OR = 2.30, 95% CI (1.91-2.69)), and decreased rate of the 17 repeat allele (P = 0.011, OR = 0.208, 95% CI (0.098-0.439)). The present findings indicated that certain alleles or genotypes of the CNR1 gene may confer a susceptibility of schizophrenia, especially of the hebephrenic type.
引用
收藏
页码:515 / 518
页数:4
相关论文
共 35 条
[1]   CANNABIS AND SCHIZOPHRENIA - A LONGITUDINAL-STUDY OF SWEDISH CONSCRIPTS [J].
ANDREASSON, S ;
ENGSTROM, A ;
ALLEBECK, P ;
RYDBERG, U .
LANCET, 1987, 2 (8574) :1483-1486
[2]   The power of genomic control [J].
Bacanu, SA ;
Devlin, B ;
Roeder, K .
AMERICAN JOURNAL OF HUMAN GENETICS, 2000, 66 (06) :1933-1944
[3]   HALLUCINOGENIC DRUGS AS PRECIPITANTS OF SCHIZOPHRENIA [J].
BREAKEY, WR ;
GOODELL, H ;
LORENZ, PC ;
MCHUGH, PR .
PSYCHOLOGICAL MEDICINE, 1974, 4 (03) :255-261
[4]   Suggestive evidence for a schizophrenia susceptibility locus on chromosome 6q and a confirmation in an independent series of pedigrees [J].
Cao, QH ;
Martinez, M ;
Zhang, J ;
Sanders, AR ;
Badner, JA ;
Cravchik, A ;
Markey, CJ ;
Beshah, E ;
Guroff, JJ ;
Maxwell, ME ;
Kazuba, DM ;
Whiten, R ;
Goldin, LR ;
Gershon, ES ;
Gejman, PV .
GENOMICS, 1997, 43 (01) :1-8
[5]   Cannabinoid receptor gene (CNR1): Association with IV drug use [J].
Comings, DE ;
Muhleman, D ;
Gade, R ;
Johnson, P ;
Verde, R ;
Saucier, G ;
MacMurray, J .
MOLECULAR PSYCHIATRY, 1997, 2 (02) :161-168
[6]   Genetic association between alleles of pancreatic phospholipase A2 gene and bipolar affective disorder [J].
Dawson, E ;
Gill, M ;
Curtis, D ;
Castle, D ;
Hunt, N ;
Murray, R ;
Powell, J .
PSYCHIATRIC GENETICS, 1995, 5 (04) :177-180
[7]   Studies on [3H]CP-55940 binding in the human central nervous system:: Regional specific changes in density of cannabinoid-1 receptors associated with schizophrenia and cannabis use [J].
Dean, B ;
Sundram, S ;
Bradbury, R ;
Scarr, E ;
Copolov, D .
NEUROSCIENCE, 2001, 103 (01) :9-15
[8]  
DEVANE WA, 1988, MOL PHARMACOL, V34, P605
[9]   Endocannabinoids: endogenous cannabinoid receptor ligands with neuromodulatory action [J].
Di Marzo, V ;
Melck, D ;
Bisogno, T ;
De Petrocellis, L .
TRENDS IN NEUROSCIENCES, 1998, 21 (12) :521-528
[10]   Towards a cannabinoid hypothesis of schizophrenia: Cognitive impairments due to dysregulation of the endogenous cannabinoid system [J].
Emrich, HM ;
Leweke, FM ;
Schneider, U .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1997, 56 (04) :803-807