Table of Contents
ISRN Psychiatry
Volume 2012, Article ID 852949, 5 pages
http://dx.doi.org/10.5402/2012/852949
Clinical Study

Monoamine Oxidase A and B Gene Polymorphisms and Negative and Positive Symptoms in Schizophrenia

1Posgrado de Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, 03100 México, DF, Mexico
2Departmento de Genética Psiquiátrica, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, 14370 México, DF, Mexico
3Subdirección Investigaciones Clínicas, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, 14370 México, DF, Mexico
4Clínica de Genética Psiquiátrica, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, 14370 México, DF, Mexico
5División Académica Multidisciplinaria de Comalcalco, Universidad Juárez Autónoma de Tabasco, 86040 Comalcalco, Tabasco, Mexico
6Servicios de Atención Psiquiátrica, Secretaría de Salud y Grupo Médico Carracci, Carracci 107, 03740 México, DF, Mexico

Received 7 February 2012; Accepted 27 February 2012

Academic Editors: J. Chou, C. U. Lee, and C. Toni

Copyright Β© 2012 Beatriz Camarena et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Given that schizophrenia is a heterogeneous disorder, the analysis of clinical characteristics could help to identify homogeneous phenotypes that may be of relevance in genetic studies. Linkage and association studies have suggested that a locus predisposing to schizophrenia may reside within Xp11. We analyzed uVNTR and rs1137070, polymorphisms from MAOA and rs1799836 of MAOB genes to perform single SNP case-control association study in a sample of 344 schizophrenia patients and 124 control subjects. Single polymorphism analysis of uVNTR, rs1137070 and rs1799836 SNPs did not show statistical differences between cases and controls. Multivariate ANOVA analysis of clinical characteristics showed statistical differences between MAOB/rs1799836 and affective flattening scores ( 𝐹 = 4 . 8 5 2 , 𝑃 = 0 . 0 0 9 ), and significant association between MAOA/uVNTR and affective flattening in female schizophrenia patients ( 𝐹 = 4 . 2 3 6 , 𝑃 = 0 . 0 1 6 ) after Bonferroni’s correction. Our preliminary findings could suggest that severity of affective flattening may be associated by modifier variants of MAOA and MAOB genes in female Mexican patients with schizophrenia. However, further large-scale studies using quantitative symptom-based phenotypes and several candidate variants should be analyzed to obtain a final conclusion.