Possible association of the MAG locus with schizophrenia in a Chinese Han cohort of family trios
Neurotransmitter-based hypotheses have so far led to only moderate success in predicting new pathogenetic findings in etiology of schizophrenia. On the other hand, the more recent oligodendroglia hypotheses of this disorder have been supported by an increasing body of evidence. For example, the expr...
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Published in: | Schizophrenia research Vol. 75; no. 1; pp. 11 - 19 |
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Main Authors: | , , , , , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Amsterdam
Elsevier B.V
01-06-2005
Elsevier Science |
Subjects: | |
Online Access: | Get full text |
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Summary: | Neurotransmitter-based hypotheses have so far led to only moderate success in predicting new pathogenetic findings in etiology of schizophrenia. On the other hand, the more recent oligodendroglia hypotheses of this disorder have been supported by an increasing body of evidence. For example, the expression level of the myelin associated glycopretein (
MAG) gene has been shown to be significantly lower in schizophrenia patient groups compared to control groups. Such an effect might be a result of genetic variations of the
MAG gene. In order to test this hypothesis, we genotyped four markers within the
MAG locus in 413 trios sample of the Han Chinese using allele-specific PCR. None of the four markers revealed noticeable allelic significance. However, the four-marker and two-marker haplotypes covering components rs720309 and rs720308 were observed to be significantly associated with schizophrenia (
P<0.0001) in this study. In addition, we identified one common risk haplotype TA (rs720309–rs720308, present in 78.5% of the general population) that showed increased evidence of overtransmission from parents to affected offspring (
P=0.0001). The results demonstrated
MAG might play a role in genetic susceptibility to schizophrenia. Furthermore, our finding of a possible association between the
MAG locus and schizophrenia is in agreement with the hypotheses of oligodendrltic and myelination dysfunction. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0920-9964 1573-2509 |
DOI: | 10.1016/j.schres.2004.11.013 |