TY  - JOUR
AB  - The XXIIIrd World Congress of Psychiatric Genetics meeting, sponsored by the International Society of Psychiatric Genetics, was held in Toronto, ON, Canada, on 16-20 October 2015. Approximately 700 participants attended to discuss the latest state-of-the-art findings in this rapidly advancing and evolving field. The following report was written by trainee travel awardees. Each was assigned one session as a rapporteur. This manuscript represents the highlights and topics that were covered in the plenary sessions, symposia, and oral sessions during the conference, and contains major notable and new findings.
AU  - Zai, G.*
AU  - Alberry, B.*
AU  - Knauer-Arloth, J.
AU  - Bánlaki, Z.*
AU  - Bares, C.*
AU  - Boot, E.*
AU  - Camilo, C.*
AU  - Chadha, K.*
AU  - Chen, Q.*
AU  - Cole, C.B.*
AU  - Cost, K.T.*
AU  - Crow, M.*
AU  - Ekpor, I.*
AU  - Fischer, S.B.*
AU  - Flatau, L.*
AU  - Gagliano, S.*
AU  - Kirli, U.*
AU  - Kukshal, P.*
AU  - Labrie, V.*
AU  - Lang, M.*
AU  - Lett, T.A.*
AU  - Maffioletti, E.*
AU  - Maier, R.*
AU  - Mihaljevic, M.*
AU  - Mittal, K.*
AU  - Monson, E.T.*
AU  - O'Brien, N.L.*
AU  - Østergaard, S.D.*
AU  - Ovenden, E.*
AU  - Patel, S.*
AU  - Peterson, R.E.*
AU  - Pouget, J.G.*
AU  - Rovaris, D.L.*
AU  - Seaman, L.*
AU  - Shankarappa, B.*
AU  - Tsetsos, F.*
AU  - Vereczkei, A.*
AU  - Wang, C.*
AU  - Xulu, K.*
AU  - Yuen, R.K.*
AU  - Zhao, J.*
AU  - Zai, C.C.*
AU  - Kennedy, J.L.*
C1  - 52946
C2  - 42215
SP  - 229-257
TI  - Rapporteur summaries of plenary, symposia, and oral sessions from the XXIIIrd World Congress of Psychiatric Genetics Meeting in Toronto, Canada, 16-20 October 2015.
JO  - Psychiatr. Genet.
VL  - 26
IS  - 6
PY  - 2016
SN  - 0955-8829
ER  - 

TY  - JOUR
AU  - Nassab, M.H.*
AU  - Rhein, M.*
AU  - Heese, P.*
AU  - Glahn, A.*
AU  - Frieling, H.*
AU  - Linnebank, M.*
AU  - Bleich, S.*
AU  - Kornhuber, J.*
AU  - Heberlein, A.*
AU  - Grallert, H.
AU  - Peters, A.
AU  - Rawal, R.
AU  - Strauch, K.
AU  - Hillemacher, T.*
C1  - 42828
C2  - 35539
CY  - Philadelphia
SP  - 41-42
TI  - No association between the ALDH2 promoter polymorphism rs886205, alcohol dependence, and risky alcohol consumption in a German population.
JO  - Psychiatr. Genet.
VL  - 25
IS  - 1
PB  - Lippincott Williams & Wilkins
PY  - 2015
SN  - 0955-8829
ER  - 

TY  - JOUR
AB  - OBJECTIVES: Genomewide association studies (GWAS) have identified clear evidence of genetic markers for nicotine dependence. Other smoking phenotypes have been tested, but the results are less consistent. The tendency to relapse versus the ability to maintain long-term abstinence has received little attention in genetic studies; thus, our aim was to provide a better biological understanding of this phenotype through the identification of genetic loci associated with smoking relapse. METHODS: We carried out a GWAS on data from two European population-based collections, including a total of 835 cases (relapsers) and 990 controls (abstainers). Top-ranked findings from the discovery phase were tested for replication in two additional independent European population-based cohorts. RESULTS: Of the seven top markers from the discovery phase, none were consistently associated with smoking relapse across all samples and none reached genomewide significance. A single-nucleotide polymorphism rs1008509, within the Xylosyltransferase II (XYLT2) gene, was suggestively associated with smoking relapse in the discovery phase (β=-0.504; P=5.6E-06) and in the first replication sample (ALSPAC) (β=-0.27; P=0.004; n=1932), but not in the second sample (KORA) (β=0.19; P=0.138; n=912). We failed to identify an association between loci implicated previously in other smoking phenotypes and smoking relapse. CONCLUSION: Although no genomewide significant findings emerged from this study, we found that loci implicated in other smoking phenotypes were not associated with smoking relapse, which suggests that the neurobiology of smoking relapse and long-term abstinence may be distinct from biological mechanisms implicated in the development of nicotine dependence.
AU  - Tozzi, F.*
AU  - Teumer, A.*
AU  - Munafò, M.*
AU  - Rawal, R.
AU  - Kazeem, G.*
AU  - Gerbaulet, M.*
AU  - McArdle, W.*
AU  - Chilcoat, H.*
AU  - Döring, A.
AU  - Dahmen, N.*
AU  - Mooser, V.*
AU  - Nauck, M.*
AU  - Ring, S.M.*
AU  - Rubio, J.P.*
AU  - Vollenweider, P.*
AU  - Waeber, G.*
AU  - John, U.*
AU  - Völzke, H.*
AU  - Homuth, G.*
AU  - Freyberger, H.J.*
AU  - Völker, U.*
AU  - Davey Smith, G.*
AU  - Gieger, C.
AU  - Preisig, M.*
AU  - Grabe, H.J.*
C1  - 25230
C2  - 31851
SP  - 143-152
TI  - A genomewide association study of smoking relapse in four European population-based samples.
JO  - Psychiatr. Genet.
VL  - 23
IS  - 4
PB  - Lippincott Williams & Wilkins
PY  - 2013
SN  - 0955-8829
ER  - 

TY  - JOUR
AB  - Genetic variation in glutamatergic signalling pathways is believed to play a substantial role in the aetiology of schizophrenia. The N-methyl-D-aspartate receptor subunit gene GRIN1 has been proposed as a candidate gene for schizophrenia. We tested for a potential association between schizophrenia and four single nucleotide polymorphisms (rs4880213, rs11146020, rs6293, and rs10747050) and one microsatellite marker at GRIN1 in a German sample of 354 patients and 323 controls. We found significant associations in single-marker and haplotype-based analyses (P<0.05). Significance was more pronounced (P<0.01) in the subset of patients with a lifetime history of major depression, a subgroup of schizophrenia described previously as a promising phenotypic subtype in genetic studies of schizophrenia. Although significances did not withstand correction for multiple testing, the results of our exploratory analysis warrant further studies on GRIN1 and schizophrenia.
AU  - Georgi, A.*
AU  - Abou Jamra, R.*
AU  - Klein, K.*
AU  - Villela, A.W.*
AU  - Schumacher, J.*
AU  - Becker, T.*
AU  - Paul, T.*
AU  - Schmael, C.*
AU  - Höfels, S.
AU  - Klopp, N.
AU  - Illig, T.
AU  - Propping, P.*
AU  - Cichon, S.*
AU  - Nöthen, M.M.*
AU  - Schulze, T.G.*
AU  - Rietschel, M.*
C1  - 766
C2  - 24944
SP  - 308-310
TI  - Possible association between genetic variants at the GRIN1 gene and schizophrenia with lifetime history of depressive symptoms in a German sample.
JO  - Psychiatr. Genet.
VL  - 17
IS  - 5
PB  - Lippincott Williams & Wilkins
PY  - 2007
SN  - 0955-8829
ER  - 

TY  - JOUR
AU  - Schirmbeck, F.*
AU  - Georgi, A.*
AU  - Strohmaier, J.*
AU  - Schmael, C.*
AU  - Knorr, C.*
AU  - Jamra, R.A.*
AU  - Schumacher, J.*
AU  - Becker, T.*
AU  - Klopp, N.
AU  - Illig, T.
AU  - Wulf, M.*
AU  - Schwarz, M.*
AU  - Maier, W.*
AU  - Propping, P.*
AU  - Cichon, S.*
AU  - Nöthen, M.M.*
AU  - Schulze, T.G.*
AU  - Rietschel, M.*
C1  - 3200
C2  - 24627
SP  - 127
TI  - No association between the serine racemase gene (SRR) and bipolar disorder in a German case-control sample.
JO  - Psychiatr. Genet.
VL  - 17
IS  - 2
PB  - Lippincott Williams & Wilkins
PY  - 2007
SN  - 0955-8829
ER  - 

TY  - JOUR
AU  - Strohmaier, J.*
AU  - Georgi, A.*
AU  - Schirmbeck, F.*
AU  - Schmael, C.*
AU  - Abou Jamra, R.*
AU  - Schumacher, J.*
AU  - Becker, T.*
AU  - Höfels, S.*
AU  - Klopp, N.
AU  - Illig, T.
AU  - Propping, P.*
AU  - Cichon, S.*
AU  - Nöthen, M.M.*
AU  - Rietschel, M.*
AU  - Schulze, T.G.*
C1  - 1552
C2  - 24628
SP  - 125
TI  - No association between the serine racemase gene (SRR) and schizophrenia in a German case-control sample.
JO  - Psychiatr. Genet.
VL  - 17
IS  - 2
PB  - Lippincott Williams & Wilkins
PY  - 2007
SN  - 0955-8829
ER  - 

TY  - JOUR
AB  - Disturbed glutamatergic neurotransmission has been implicated in the pathogenesis of schizophrenia and bipolar disorder, with the N-methy-D-aspartate receptors being in the focus of research. The NR1 subunit, which is encoded by the gene GRIN1, plays a key role in the functionality of N-methy-D-aspartate receptors. We tested the association between GRIN1 and bipolar disorder in a sample of German descent, consisting of 306 bipolar disorder patients and 319 population-based controls. No significant association was found. In accordance with our recent findings, we hypothesized that restricting case definition to individuals with a history of persecutory delusions might clarify the relationship between bipolar disorder and GRIN1. This stratified analysis did not yield any significant association either. Our results do not support an association of the GRIN1 gene with bipolar disorder in the German population. © 2006 Lippincott Williams & Wilkins.
AU  - Georgi, A.*
AU  - Jamra, R.A.*
AU  - Schumacher, J.*
AU  - Becker, T.*
AU  - Schmael, C.*
AU  - Deschner, M.*
AU  - Höfels, S.*
AU  - Wulff, M.*
AU  - Schwarz, M.*
AU  - Klopp, N.
AU  - Illig, T.
AU  - Propping, P.*
AU  - Cichon, S.*
AU  - Nöthen, M.M.*
AU  - Rietschel, M.*
AU  - Schulze, T.G.*
C1  - 5801
C2  - 24282
SP  - 183-184
TI  - No association between genetic variants at the GRIN1 gene and bipolar disorder in a Germany sample.
JO  - Psychiatr. Genet.
VL  - 16
IS  - 5
PY  - 2006
SN  - 0955-8829
ER  - 

TY  - JOUR
AU  - Jamra, R.A.*
AU  - Villela, A.W.*
AU  - Klein, K.*
AU  - Becker, T.*
AU  - Schulze, T.G.*
AU  - Schmael, C.*
AU  - Deschner, M.*
AU  - Klopp, N.
AU  - Illig, T.
AU  - Propping, P.*
AU  - Cichon, S.*
AU  - Rietschel, M.*
AU  - Nöthen, M.M.*
AU  - Schumacher, J.*
C1  - 5802
C2  - 24283
SP  - 91
TI  - No association between genetic variants at the GLYT2 gene and bipolar affective disorder and schizophrenia.
JO  - Psychiatr. Genet.
VL  - 16
IS  - 3
PY  - 2006
SN  - 0955-8829
ER  - 

TY  - JOUR
AB  - Altered glutamatergic neurotransmission is considered a potential etiological factor of schizophrenia (SCZ) and affective disorders. The gene ASCT1 (SLC1A4) coding for a Na-dependent neutral aminoacid transporter is a member of the glutamate transporter superfamily and is located on 2p13-14, a region showing linkage to both SCZ and bipolar disorder (BD). ASCT1 can thus be considered a candidate gene for both disorders. In a German sample, we tested for association between ASCT1 and both SCZ and BD. Allele and haplotype frequencies, however, did not differ between cases and controls. Recent findings on the associations between brainderived neurotrophic factor (BDNF) and SCZ and between G72/G30 and BD suggest that SCZ patients with a history of major depressive episodes (MDE) outside psychotic episodes and BD cases with a history of persecutory delusions constitute genetically distinct subgroups of these disorders. Thus, we hypothesized that restricting case definition to those 95 SCZ individuals with MDE and to those 107 BD patients with a history of persecutory delusions might clarify the relationship between BD, SCZ and ASCT1. However, these stratification approaches did not yield any significant association either. Allele and haplotype frequencies did not differ between cases and controls. Our results do not support an association of the ASCT1 gene with BD or SCZ in the German population.
AU  - Skowronek, M.H.*
AU  - Georgi, A.*
AU  - Jamra, R.A.*
AU  - Schumacher, J.*
AU  - Becker, T.*
AU  - Schmael, C.*
AU  - Paul, T.*
AU  - Deschner, M.*
AU  - Höfels, S.*
AU  - Wulff, M.*
AU  - Schwarz, M.*
AU  - Klopp, N.
AU  - Illig, T.
AU  - Propping, P.*
AU  - Cichon, S.*
AU  - Nöthen, M.M.*
AU  - Schulze, T.G.*
AU  - Rietschel, M.*
C1  - 5877
C2  - 24496
SP  - 233-234
TI  - No association between genetic variants at the ASCT1 gene and schizophrenia or bipolar disorder in a German sample.
JO  - Psychiatr. Genet.
VL  - 16
IS  - 6
PY  - 2006
SN  - 0955-8829
ER  -