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PCM1 and schizophrenia: A replication study in the Northern Swedish population
Author(s) -
Moens Lotte N.,
Ceulemans Shana,
Alaerts Maaike,
Van Den Bossche Maarten J.A.,
Lenaerts AnSofie,
De Zutter Sonia,
Norrback KarlFredrik,
Adolfsson Rolf,
DelFavero Jurgen
Publication year - 2010
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.31088
Subject(s) - haplotype , single nucleotide polymorphism , schizophrenia (object oriented programming) , population , snp , replication (statistics) , genetics , genetic association , biology , allele , medicine , psychiatry , genotype , gene , virology , environmental health
Previous studies implicated centrosomal dysfunction as a source of various neuropsychiatric disorders, including schizophrenia (SZ). Two recent reports [Gurling et al., 2006; Datta et al., 2008. Mol Psychiatry] described an association between polymorphisms in the PCM1 gene and SZ in a UK/Scottish population. In this study, we aimed to replicate these findings in a Northern Swedish association sample of 486 research subjects with SZ and 512 unrelated control individuals. We genotyped 12 previously described SNP markers and carried out haplotype analyses using the same multi‐marker haplotypes previously reported. Though we could not replicate the association with SNPs rs445422 and rs208747, we did observe a significant protective association with intronic SNP rs13276297. Furthermore, we performed a meta‐analysis comprising 1,794 SZ patients and 1,553 controls, which confirmed the previously reported association with rs445422 and rs208747. These data provide further evidence that PCM1 —though certainly not a major risk factor in the Northern Swedish population—cannot be ruled out as a contributor to SZ risk and/or protection, and deserves further replication in larger populations to elucidate its role in disease etiology. © 2010 Wiley‐Liss, Inc.