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MAOA Interacts With the ALDH2 Gene in Anxiety–Depression Alcohol Dependence
Author(s) -
Lee ShengYu,
Hahn ChengYi,
Lee JiaFu,
Huang SanYuan,
Chen ShiouLan,
Kuo PoHsiu,
Lee I Hui,
Yeh Tzung Lieh,
Yang Yen Kuang,
Chen ShihHeng,
Ko HueiChen,
Lu RuBand
Publication year - 2010
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2010.01198.x
Subject(s) - monoamine oxidase a , aldh2 , anxiety , alcohol dependence , medicine , psychiatry , depression (economics) , genotype , psychology , clinical psychology , genetics , alcohol , biology , gene , serotonin , biochemistry , receptor , macroeconomics , economics
Background: Alcohol dependence is usually comorbid with anxiety disorder, depressive disorder, or both; this comorbidity may increase drinking behavior. We previously hypothesized that anxiety–depressive alcohol dependence (ANX/DEP ALC) was a genetically specific subtype of alcohol dependence. ANX/DEP ALC may be related to dopamine and serotonin, which are catalyzed by monoamine oxidase A (MAOA) and acetaldehyde dehydrogenase 2 (ALDH2). The aim of this study was to determine whether the interaction between the MAOA and the ALDH2 genes is associated with ANX/DEP ALC. Methods: We recruited 383 Han Chinese men in Taiwan: 143 ANX/DEP ALC and 240 healthy controls. The diagnosis of ANX/DEP ALC (alcohol dependence with a past or current history of anxiety, depressive disorder, or both) was made using DSM‐IV criteria. Genotypes of ALDH2 and MAOA‐uVNTR (variable number of tandem repeat located upstream) were determined using PCR‐RFLP. Results: The ALDH2 , but not the MAOA‐uVNTR , polymorphism was associated with ANX/DEP ALC. After stratifying the MAOA‐uVNTR polymorphism, we found a stronger association between the ALDH2*1/*2 and *2/*2 genotypes and the controls in the MAOA‐uVNTR 4‐repeat subgroup. Logistic regression significantly associated the interaction between ALDH2 and MAOA variants with ANX/DEP ALC. Conclusion: We conclude that the MAOA and ALDH2 genes interact in ANX/DEP ALC. Although the MAOA gene alone is not associated with ANX/DEP ALC, we hypothesize that different variants of MAOA‐uVNTR polymorphisms modify the protective effects of the ALDH2*2 allele on ANX/DEP ALC in Han Chinese in Taiwan.