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A functional promoter polymorphism (-116C/G) of the X-box binding protein 1 gene (XBP1) gene was reported to be associated with schizophrenia in Asian subjects. In a replication attempt, three European case-control samples comprising 2,182 German, Polish, and Swedish subjects, were genotyped for the XBP1 -116C/G polymorphism. Allele and genotype frequencies were compared between schizophrenic patients and control subjects. There were no significant case-control differences in any of the three samples, although in a meta-analysis with previous results comprising 3,612 subjects there was a borderline association between the -116G-containing genotypes and schizophrenia. We conclude that the functional XBP1 gene polymorphism is not of major importance to schizophrenia in the European populations investigated. It cannot be excluded, however, that the XBP1 polymorphism is involved in schizophrenia in other populations or adds minor susceptibility to the disorder.

Erratum ‘‘Association Study of a Functional Promoter Polymorphism in the XBP1 Gene and Schizophrenia,’’ American Journal Of Medical Genetics Part B (Neuropsychiatric Genetics) 141B:71–75 (2006) Erik G. Jonsson, Sven Cichon, Johannes Schumacher, Rami Abou Jamra, Thomas G. Schulze, Monica Deschner, Kaj Forslund, Hakan Hall, Peter Propping, Piotr M. Czerski, Monika Dmitrzak-Weglarz, Pawel Kapelski, Martin Driessen, Wolfgang Maier, Joanna Hauser, Marcella Rietschel, and Markus M. Nothen Department of Clinical Neuroscience, Psychiatry Section, Karolinska Institutet, Stockholm, Sweden Institute of Human Genetics, University of Bonn, Bonn, Germany Life & Brain Center, University of Bonn, Bonn, Germany Division of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Mannheim, Germany Department of Adult Psychiatry, Poznan University of Medical Sciences, Poznan, Poland Department of Psychiatry, Gilead Hospital, v. Bodelschwingsche Anstalten Bethel, Bielefeld, Germany Department of Psychiatry, University of Bonn, Bonn, Germany

Results from molecular and pharmacological studies point to involvement of the gene coding for the phosphatidylinositol-4-phosphate 5-kinase type II-alpha (PIP5K2A) in the development of schizophrenia and bipolar affective disorder (BPAD). The PIP5K2A gene locus, which is located on chromosomal region 10p12, has been implicated in the development of both disorders by independent linkage and association studies. On a cellular level, PIP5K2A is an enzyme component of the metabolism of inositol phosphate, which has been considered a potential target for the therapeutic action of lithium in BPAD patients. Given that the PIP5K2A gene is a promising candidate for the development of both disorders, we performed an association study between genetic variants at the PIP5K2A locus and 268 patients with schizophrenia, 260 patients with BPAD and 325 ethnically matched healthy controls. We failed to detect association to either disorder using PIP5K2A gene variants through single-marker and haplotype analysis. Therefore, our data does not support an involvement of the PIP5K2A locus in the etiology of either schizophrenia or BPAD in the German population. © 2006 Wiley-Liss, Inc.

Several lines of evidence suggest an involvement of the noradrenergic neurotransmitter system in the pathogenesis of bipolar affective disorder (BPAD). Three genes for alpha-adrenergic receptors (ADRA) are located in chromosomal regions that showed evidence for linkage: The alpha(1c)-adrenergic (ADRA-1C) receptor gene on 8p21, the alpha(2a)-adrenergic (ADRA-2A) receptor gene on 10q25, and the alpha(2c)-adrenergic (ADRA-2C) receptor on 4p16. In a BPAD sample of 120 parent-offspring triads, we genotyped a 492 Cys/Arg variant in exon 2 of the ADRA-1C gene, a -1291 G/C variant in the 5'UTR of the ADRA-2A gene, and a STR marker (adra2c1) in the 5'UTR of the ADRA-2C gene. Using the Transmission Disequilibrium Test (TDT), no significant differences in transmissions were observed for any of the three ADRA genes.