NDLI: Effects of MAOA promoter methylation on susceptibility to paranoid schizophrenia

Content Provider	Springer Nature Link
Author	Chen, Yanbo Zhang, Jiexu Zhang, Li Shen, Yan Xu, Qi
Copyright Year	2011
Abstract	This study was undertaken to analyze DNA methylation profiling at the monoamine oxidase A (MAOA) locus, in order to determine whether abnormal DNA methylation is involved in the development of schizophrenia. We recruited a total of 371 patients with paranoid schizophrenia (199 males and 172 females) and 288 unrelated control subjects (123 males and 165 females) for analysis of DNA methylation. Diagnosis was made based on the Structured Clinical Interview for DSM-VI. Genomic DNA extracted from peripheral blood was chemically modified using bisulfite, and DNA methylation profiles of the MAOA promoter were determined by BSP-sequencing. DNA methylation ratios of individual CpG residues and overall methylation ratios were measured on each subject. The results showed that there was no significant difference in overall DNA methylation ratios between patients and controls either in the female group (P = 0.42) or in the male group (P = 0.24). Of 15 CpG residues that showed significant differences in DNA methylation status between the patient group and the control group in females, eight of which had an increased level and seven, a decreased level, with a combined P value of 1 (df = 160). In male subjects, however, six individual CpG residues showed an increased methylation level with a combined P value of 5.80E−35 (df = 158). In conclusion, abnormalities of DNA methylation at the MAOA promoter may be associated with schizophrenia in males.
Starting Page	1081
Ending Page	1087
Page Count	7
File Format	PDF
ISSN	03406717
Journal	Human Genetics
Volume Number	131
Issue Number	7
e-ISSN	14321203
Language	English
Publisher	Springer-Verlag
Publisher Date	2011-12-24
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Metabolic Diseases Molecular Medicine Gene Function Human Genetics
Content Type	Text
Resource Type	Article
Subject	Genetics Genetics (clinical)

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