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P.1.a.014 No association of CCK promoter gene −36C>T polymorphism and panic disorder in the Korean population
P.1.a Basic neuroscience – Genetics and genomics rs4680, rs165599, there was no significant odds ratio between schizophrenics and normal controls. There was no significant differences between schizophrenics and normal controls in the frequency of allele for the four SNPs of the COMT gene, the frequency of genotype for the four SNPs of the COMT gene and the frequency of haplotype. Gene variation of MTHFR C677T, A1298C was analysised, but we can not find any significant differences of gene-distribution, alleles distribution, genotype and haplotype. And we also cannot find the significant differences between their alleles and onset-age in MTHFR C677T, A1298C. Conclusion: Genetic association between four SNPs on COMT gene and Korean schizophrenics was generally not to be found in this study but our finding is suggestive of genetic components for gender-specificity and onset age in Korean schizophrenics. We suggest that MTHFR C677T, MTHFR A1298C genotypes are not related to the risk factors for schizophrenia References [1] Daniels NM, Williams J, Jones LA, Cardno AG, Murhy KC, Spurlock G, Riley B, Scambler P, Asherson P, McGuffin P, Owen MJ, 1996, NO evidence for allelic association between schizophrenia and a polymorphism determining high or low catechol-O-methyltransferase activity. Am J Psychiatry 153, 268–270. [2] Karayiorgou M, Gogos JA, Galke BL, Wolyniec PS, Nestadt G, Antonarakis SE, Kazazian HH, Housman DE, Pulver AE, 1998, Identification of sequence variants and analysis of the role of the catechol-Omethyltransferase gene in schizophrenia susceptibility. Biol Psychiatry 43, 425–431. [3] Strous RD, Bark N, Woerner M, Lachman HM, 1997 Lack of association of a functional catechol-O-methyltransferase gene polymorphism in schizophrenia. Biol Psychiatry 41, 493–495.
P.1.a.014 No association of CCK promoter gene −36C>T polymorphism and panic disorder in the Korean population
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attack scores during the previous one month, as well as scores for anticipatory anxiety, panic distress, and agoraphobic distress, as determined by a visual analogue scale (VAS). And all the subjects were recommended to complete the measures such as STAI-S, STAI-T, BDI, SCL-90-R, ASI-R, CGI-S, PDSS, and (HAMD). Responder analyses were conducted on the basis of changes in CGI-I scores after 10 weeks of treatment. Results: The distribution of genotype is within the range of Hardy-Weinberg equilibrium in both panic group and control. Genotype and allele distribution of CCK promoter −36C>T polymorphism patients with panic disorder was not significantly different from those of the controls. In addition, after excluding panic disorder patients with major depressive disorder, we did not find out the association of CCK −36C>T with the panic disorder without comorbidities. In analysis for determine the difference of 10 week-pharmacotherapeutic response according to genotype, CGI-I scores did not significantly differ among the genotypes of CCK promoter −36C>T polymorphism. When we subdivided the patients into responders (CGI-I: 1−2) and non-responders (CGI-I: 3−7), we found no differences between the groups with regard to genotypic and allelic frequencies. Conclusion: This study suggested that the CCK promoter −36C>T polymorphism may have not a potential role for susceptibility to panic disorder in the Korean population. And the response to 10 week-pharmacotherapy is not different according to the genotype of CCK promoter −36C>T polymorphism. Thus calls for consecutive studies in order to pile up the data with larger different ethnic background. References [1] Wang Z, Valdes J, Noyes R, Zoega T, Crowe RR, 1998, Possible association of a cholecystokinin promoter polymorphism (CCK-36CT) with panic disorder. Am J Med Genet (Neuropshchiatr Genet) 81, 228– 234. [2] Kennedy JL, Bradwejn J, Koszychi D, King N, Crowe R, Vincent J, et al, 1999, Investigation of cholecystokinin system genes in panic disorder. Mol Psychiatry 4, 284–285.
W. Kim ° , J.M. Woo. Seoul Paik Hospital, Department of Psychiatry, Seoul, South-Korea Objective: Panic disorder is a common anxiety disorder with a lifetime prevalence of 1−3%, and characterized as many somatic symptoms combined with severe anxiety, including fears of going crazy or dying. There were researches about the biological basis of panic disorder, which suggested some physiological factors are closely related with panic attack or susceptibility of anxiety. Lactate infusion, m-chlorophenylpiperazine infusion, tryptophan depletion and cholecystokinin infusion is known to induce anxiety. Among these, cholecyctokinin (CCK), peptide located mainly in brain and digestive system, is reported to have interactions with dopamine and related with various physiologic properties such as anxiety, appetite, respiration, sleep. Some genetic polymorphisms of these anxiety-related physiologic agents have been reported to related with panic disorder. Recently, possible association of CCK promoter gene −36C>T was reported in Caucasian. Therefore, we aimed to test the possible association between cholecystokinin(CCK) promoter gene −36C>T polymorphism and panic disorder in Korean population. Methods: 267 patients with panic disorder and 82 healthy controls participated in this study. Genotyping was performed by polymerase chain reaction-based method. Chip-based MALDITOF (matrix assisted laser desorption ionization time of flight) mass spectrometry platform was applied in analysis. The severity of the patients’ panic disorders was assessed according to panic
P.1.a.015 Neuregulin-1 risk haplotype and eye movements in schizophrenia M. Haraldsson1 ° , U. Ettinger2 , B.B. Magnusdottir1 , T. Sigmundsson1 , E. Sigurdsson1 , H. Petursson1 . 1 LandspitaliUniversity Hospital, Psychiatry, Reykjavik, Iceland; 2 Institute of Psychiatry, Center for Neuroimaging Sciences, London, United Kingdom Aim: To investigate effects of the Neuregulin-1 (NRG-1) “atrisk” haplotype on antisaccade (AS) and smooth pursuit (SP) eye movements in schizophrenia patients and healthy controls. Background: Recent studies provide evidence for an association between variations in the NRG-1 gene and schizophrenia (Stefansson et al. 2002). NRG-1 has multiple roles in the central nervous system including neuronal migration, synapse formation and expression of the NMDA glutamate receptor. The phenotypic heterogeneity of schizophrenia complicates studies of how NRG-1 and other potential risk genotypes affect the disease phenotype. This problem may be circumvented by studying endophenotypes. Endophenotypes are biological or behavioural features which may be more closely related to underlying disease genes than the complex clinical phenotype (Braff et al. 2007). Deficits in AS and SP eye movements are promising endophenotypes in genetic studies
P.1.a.014 No association of CCK promoter gene −36C>T polymorphism and panic disorder in the Korean population
S235
attack scores during the previous one month, as well as scores for anticipatory anxiety, panic distress, and agoraphobic distress, as determined by a visual analogue scale (VAS). And all the subjects were recommended to complete the measures such as STAI-S, STAI-T, BDI, SCL-90-R, ASI-R, CGI-S, PDSS, and (HAMD). Responder analyses were conducted on the basis of changes in CGI-I scores after 10 weeks of treatment. Results: The distribution of genotype is within the range of Hardy-Weinberg equilibrium in both panic group and control. Genotype and allele distribution of CCK promoter −36C>T polymorphism patients with panic disorder was not significantly different from those of the controls. In addition, after excluding panic disorder patients with major depressive disorder, we did not find out the association of CCK −36C>T with the panic disorder without comorbidities. In analysis for determine the difference of 10 week-pharmacotherapeutic response according to genotype, CGI-I scores did not significantly differ among the genotypes of CCK promoter −36C>T polymorphism. When we subdivided the patients into responders (CGI-I: 1−2) and non-responders (CGI-I: 3−7), we found no differences between the groups with regard to genotypic and allelic frequencies. Conclusion: This study suggested that the CCK promoter −36C>T polymorphism may have not a potential role for susceptibility to panic disorder in the Korean population. And the response to 10 week-pharmacotherapy is not different according to the genotype of CCK promoter −36C>T polymorphism. Thus calls for consecutive studies in order to pile up the data with larger different ethnic background. References [1] Wang Z, Valdes J, Noyes R, Zoega T, Crowe RR, 1998, Possible association of a cholecystokinin promoter polymorphism (CCK-36CT) with panic disorder. Am J Med Genet (Neuropshchiatr Genet) 81, 228– 234. [2] Kennedy JL, Bradwejn J, Koszychi D, King N, Crowe R, Vincent J, et al, 1999, Investigation of cholecystokinin system genes in panic disorder. Mol Psychiatry 4, 284–285.
W. Kim ° , J.M. Woo. Seoul Paik Hospital, Department of Psychiatry, Seoul, South-Korea Objective: Panic disorder is a common anxiety disorder with a lifetime prevalence of 1−3%, and characterized as many somatic symptoms combined with severe anxiety, including fears of going crazy or dying. There were researches about the biological basis of panic disorder, which suggested some physiological factors are closely related with panic attack or susceptibility of anxiety. Lactate infusion, m-chlorophenylpiperazine infusion, tryptophan depletion and cholecystokinin infusion is known to induce anxiety. Among these, cholecyctokinin (CCK), peptide located mainly in brain and digestive system, is reported to have interactions with dopamine and related with various physiologic properties such as anxiety, appetite, respiration, sleep. Some genetic polymorphisms of these anxiety-related physiologic agents have been reported to related with panic disorder. Recently, possible association of CCK promoter gene −36C>T was reported in Caucasian. Therefore, we aimed to test the possible association between cholecystokinin(CCK) promoter gene −36C>T polymorphism and panic disorder in Korean population. Methods: 267 patients with panic disorder and 82 healthy controls participated in this study. Genotyping was performed by polymerase chain reaction-based method. Chip-based MALDITOF (matrix assisted laser desorption ionization time of flight) mass spectrometry platform was applied in analysis. The severity of the patients’ panic disorders was assessed according to panic
P.1.a.015 Neuregulin-1 risk haplotype and eye movements in schizophrenia M. Haraldsson1 ° , U. Ettinger2 , B.B. Magnusdottir1 , T. Sigmundsson1 , E. Sigurdsson1 , H. Petursson1 . 1 LandspitaliUniversity Hospital, Psychiatry, Reykjavik, Iceland; 2 Institute of Psychiatry, Center for Neuroimaging Sciences, London, United Kingdom Aim: To investigate effects of the Neuregulin-1 (NRG-1) “atrisk” haplotype on antisaccade (AS) and smooth pursuit (SP) eye movements in schizophrenia patients and healthy controls. Background: Recent studies provide evidence for an association between variations in the NRG-1 gene and schizophrenia (Stefansson et al. 2002). NRG-1 has multiple roles in the central nervous system including neuronal migration, synapse formation and expression of the NMDA glutamate receptor. The phenotypic heterogeneity of schizophrenia complicates studies of how NRG-1 and other potential risk genotypes affect the disease phenotype. This problem may be circumvented by studying endophenotypes. Endophenotypes are biological or behavioural features which may be more closely related to underlying disease genes than the complex clinical phenotype (Braff et al. 2007). Deficits in AS and SP eye movements are promising endophenotypes in genetic studies