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Genetic study of the myelin oligodendrocyte glycoprotein (MOG) gene in schizophrenia
Author(s) -
Zai G.,
King N.,
Wigg K.,
Couto J.,
Wong G. W. H.,
Honer W. G.,
Barr C. L.,
Kennedy J. L.
Publication year - 2005
Publication title -
genes, brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.315
H-Index - 91
eISSN - 1601-183X
pISSN - 1601-1848
DOI - 10.1111/j.1601-183x.2004.00089.x
Subject(s) - haplotype , transmission disequilibrium test , genotype , allele , schizophrenia (object oriented programming) , genetics , biology , population , genetic association , linkage disequilibrium , medicine , single nucleotide polymorphism , gene , psychiatry , environmental health
Schizophrenia (SCZ) is a neuropsychiatric disorder that affects approximately 1% of the general population. The human leukocyte antigen (HLA) system has been implicated in several genetic studies of SCZ. The myelin oligodendrocyte glycoprotein ( MOG ) gene, which is located close to the HLA region, is considered a candidate for SCZ due to its association with white matter abnormalities and its importance in mediating the complement cascade. Four polymorphisms in the MOG gene (CA)n (TAAA)n, and two intronic polymorphisms, C1334T and C10991T, were investigated for the possibility of association with SCZ using 111 SCZ proband and their families. We examined the transmission of the alleles of each of these polymorphisms with the transmission disequilibrium test. We did not observe significant evidence for biased transmission of alleles at the (CA)n (χ 2  = 2.430, 6 df, P  = 0.876) (TAAA)n (χ 2  = 3.550, 5 df, P  = 0.616), C1334T (χ 2  = 0.040, 1 df, P  = 0.841) and C10991T (χ 2  = 0.154, 1 df, P  = 0.695) polymorphisms. Overall haplotype analysis using the TRANSMIT program was also not significant (χ 2  = 7.954, 9 df, P  = 0.539). Furthermore, our results comparing mean age at onset in the genotype groups using the Kruskal–Wallis Test were not significant. Our case‐control analyses (182 cases age‐, sex‐ and ethnicity‐matched with healthy controls) and combined z ‐score [(CA)n: z ‐score =−1.126, P  = 0.130; (TAAA)n: z ‐score = −0.233, P  = 0.408; C1334T: z ‐score = 0.703, P  = 0.241; C10991T: z ‐score = 0.551, P  = 0.291] were also not significant. Although our data are negative, the intriguing hypothesis for MOG in SCZ may warrant further investigation of this gene.

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