PCM1and schizophrenia: A replication study in the Northern Swedish populationHow to Cite this Article: Moens LN, Ceulemans S, Alaerts M, Van Den Bossche MJA, Lenaerts AS, De Zutter S, Norrback KF, Adolfsson R, DelFavero J. 2010. PCM1and Schizophrenia: A Replication Study in the Northern Swedish Population. Am J Med Genet Part B 153B:1240–1243.

Autor: Moens, Lotte N., Ceulemans, Shana, Alaerts, Maaike, Van Den Bossche, Maarten J.A., Lenaerts, AnSofie, De Zutter, Sonia, Norrback, KarlFredrik, Adolfsson, Rolf, DelFavero, Jurgen
Zdroj: American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics; September 2010, Vol. 153 Issue: 6 p1240-1243, 4p
Abstrakt: 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 PCM1gene and SZ in a UKScottish 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 multimarker 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 metaanalysis 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 andor protection, and deserves further replication in larger populations to elucidate its role in disease etiology. © 2010 WileyLiss, Inc.
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