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Study of a possible role of the monoamine oxidase A ( MAOA ) gene in paranoid schizophrenia among a Chinese population
Author(s) -
Sun Yuhui,
Zhang Jiexu,
Yuan Yanbo,
Yu Xin,
Shen Yan,
Xu Qi
Publication year - 2012
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.32009
Subject(s) - monoamine oxidase a , paranoid schizophrenia , schizophrenia (object oriented programming) , genetics , monoamine neurotransmitter , allele , genetic association , monoamine oxidase , variable number tandem repeat , haplotype , biology , psychosis , single nucleotide polymorphism , psychiatry , psychology , genotype , gene , serotonin , enzyme , biochemistry , receptor
Monoamine oxidase A (MAOA) is the enzyme responsible for degradation of several monoamines, such as dopamine and serotonin that are considered as being two of the most important neurotransmitters involved in the pathophysiology of schizophrenia. To study a possible role of the MAOA gene in conferring susceptibility to schizophrenia, the present study genotyped the variable number of tandem repeat (VNTR) polymorphism and 41 SNPs across this gene among 555 unrelated patients with paranoid schizophrenia and 567 unrelated healthy controls. Quantitative real‐time PCR analysis was employed to quantify expression of MAOA mRNA in 73 drug‐free patients. While none of these genotyped DNA markers showed allelic association with paranoid schizophrenia, haplotypic association was found for the VNTR‐rs6323, VNTR‐rs1137070, and VNTR‐rs6323‐rs1137070 haplotypes in female subjects. Nevertheless, no significant change of the expression of MAOA mRNA was detected in either female or male patients with paranoid schizophrenia. Our study suggests that the interaction between genetic variants within the MAOA gene may contribute to an increased risk of paranoid schizophrenia, but the precise mechanism needs further investigation. © 2011 Wiley Periodicals, Inc.