extracted from dorsolateral prefrontal cortex and compared across demographic and diagnostic variables as well as genotypic groups. Results: We identified 27 novel DNA variants not previously characterised, 75% of which were predicted to alter putative transcription factor binding sites. We found a significantly higher novel variant load in schizophrenic cases, where 24 cases had at least one novel variant compared to 14 controls (χ 2 = 10.8, p = 0.001). The majority of novel SNPs were identified around the HAPICE repeats in intron 1, however the overall nucleotide diversity was similar across all regions examined (θ = 0.0009-0.0022). In preliminary analysis, we saw no correlation between the novel variant load and the level of type I, II or III transcript expression (p=0.27, 0.88 and 0.62 respectively). We were unable to replicate the previously reported difference in type I mRNA levels between cases and controls (Hashimoto et al., 2004; Law et al., 2006). We were also unable to replicate the previously reported genotype × diagnosis interaction of rs7014762 on type III expression (ANCOVA p = 0.836) (Nicodemus et al., 2009). We did however find a significant effect of the rs3802160 genotype on type III expression in patients with schizophrenia (ANCOVA p = 0.04). The HAPICE risk haplotype showed no frequency distortion in this small Australian case-control cohort (χ 2 = 0.098, p = 0.754). Discussion: Our data revealed multiple rare SNP variants in the regulatory regions of the NRG1 gene, particularly in the HAPICE region in intron 1, which resulted in a higher novel variant load in schizophrenia. However, as these novel variants are rare, it is not clear how they may affect regulation NRG1 transcript expression. The lack of replication of the transcript expression changes previously described may reflect population differences, as illu- strated by the lack of association of the HAPICE risk haplotype in this cohort. However, evidence that distinct DNA variants may be linked to NRG1 expression in this Australian cohort confirm that specific sequence variants may be critical determinants of NRG1 expression in schizophrenia, but not in controls. Further character- isation of DNA and transcript expression variation by complimen- tary methods is required to elucidate the effect of DNA sequence variation on mRNA levels, to determine how genetic changes in NRG1 may impart disease risk. doi:10.1016/j.schres.2010.02.576 Poster 82 DYSTROBREVIN BINDING PROTEIN GENE (DTNBP1) IN BIPOLAR DISORDER: A REVIEW AND A META-ANALYSIS Darya Gaysina 1,2 , Gerome Breen 2 , Inti Pedroso 2 , Peter McGuffin 2 1 MRC Unit for Lifelong Health and Ageing, London, United Kingdom; 2 King's College London, London, United Kingdom Background: Recent studies suggest an overlap in genetic suscept- ibility of schizophrenia and bipolar disorder (BD). There is some evidence for association of the DTNBP1 gene with schizophrenia. Several studies have investigated the association between the DTNP1 and BD providing conflicting results. These studies have used a different set of genetic markers that makes a direct comparison of risk alleles/haplotypes impossible. The aim of the present study is to review and summarize the available data and provide a better overview of the role of the DTNBP1 in BD. Methods: Five case-control studies of the DTNBP1 in BD were available for the comparison and the meta-analysis: Raybould et al., 2005, Breen et al., 2006, Pae et al., 2007, Joo et al., 2007, and Gaysina et al., 2009. First, we used HapMap data for comparison the results of the case- control studies. HapMap CEU trio data and combined JPT and CHB trio data were used for selection the SNPs from the genomic region 10 kb upstream and downstream of the DTNBP1 gene. To determine tagging SNPs (tSNPs) for each of the studies we used the Haploview programme and the Tagger implementation therein. Second, a meta- analysis was conducted for DTNBP1 SNPs when the results of at least three studies were available. Odds ratios were combined using a fixed- effects model. We estimated a between study heterogeneity using the I 2 statistics. A funnel plot and Begg and Mazumdar's rank correlation test were used in order to assess publication bias. Results: We have identified the single marker or multi-marker haplotype that best captured the association signal in each study and used the data available from the HapMap project and Haploview to determine tSNP(s) in the original studies. These tSNPs were mapped onto the HAPMAP panel samples as a reference. We identified eight common haplotypes in the CEU trios and four common haplotypes in JPT+CHB with their respective frequencies. We matched the asso- ciated allele or haplotype from each study to the haplotypes derived for the HapMap samples. We demonstrated that two risk haplotypes identified in the samples of Caucasian ancestry were overlapping. Using a meta-analytic approach, six SNPs were analyzed. A higher frequency of the G allele of rs2619522 (OR=1.18, 95% CI 1.01-1.38), the T allele of rs760761 (OR=1.22; 95% CI 1.04-1.42), and the G allele of rs3213207 (OR=1.24, 95% CI 1.05-1.46) were shown in the BD group than in a control group. These associations were strengthened when the analysis was restricted to the studies of the samples of a Northern European ancestry. The funnel plot analysis provided the evidence for publication bias for rs2619522 (p = 0.09); and after a correction for publication bias the effect estimated was still significant for this SNP (p=0.016). No evidence for publication bias for rs760761 or rs3213207 was found. Discussion: This study using two different approaches provides the evidence for the DTNBP1 as a susceptibility gene for BD, especially in a Caucasian population. doi:10.1016/j.schres.2010.02.577 Poster 83 ASSOCIATION OF SCHIZOPHRENIA SUSCEPTIBILITY GENES WITH INTERMEDIATE PHENOTYPES: NEW FINDINGS FROM GENOMIC IMAGING Oliver Gruber 1 , Sarah Trost 1 , Thomas Wobrock 1 , Harald Scherk 1 , Thomas Schneider-Axmann 1 , Wolfgang Reith 2 , Jobst Meyer 3 , Peter Falkai 1 1 Centre for Translational Research in Systems Neuroscience and Clinical Psychiatry, Department of Psychiatry and Psychotherapy, Georg August University Goettingen, Germany; 2 Department of Neuror- adiology, Saarland University Homburg, Germany; 3 Department of Neurobehavioral Genetics, University of Trier, Trier, Germany Background: DISC1 and DTNBP1 have been linked to the risk for major psychosis. The aim of this study was to investigate the effects of the DISC1 Ser704Cys locus and of two single nucleotide polymorphisms of the DTNBP1 on cognition, regional brain volumes and MRS parameters in human subjects. Methods: Overall 232 subjects participated in the study. Subjects were genotyped with respect to the rs821616 SNP of the DISC1 gene and the rs2619522 and rs1018381 SNPs of the DTNBP1 gene, and underwent magnetic resonance imaging (MRI) and spectroscopy (MRS). MRI data were analyzed using both manual volumetric assessment of regions of interest and voxel-based morphometry (VBM) as implemented in SPM5. Results: Manual volumetric assessment, but not VBM revealed a significant effect of the DISC1-SNP rs821616 on hippocampus volume with Ser homozygotes having lower relative right hippocampal Abstracts 335