Possible Interaction of Alcohol Dehydrogenase and Aldehyde Dehydrogenase Genes With the Dopamine D2 Receptor Gene in Anxiety‐Depressive Alcohol Dependence

Huang, San-Yuan; Lin, Wei‐Wen; Ko, Huei Chen; Lee, Jia-Fu; Wang, Tso-Jen; Chou, Yuan-Hwa; Yin, Shih‐Jiun; Lu, Ru‐Band

doi:10.1097/01.alc.0000117832.62901.61

Cited by 142 publications

(108 citation statements)

References 109 publications

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“…Comparatively, our control subjects were assessed by an experienced psychiatrist and a welltrained psychologist via semistructured interviews using the SADS-L to exclude the presence of psychiatric disorders. Therefore, it is unlikely that our control group included any psychiatric patients that could produce a false-negative result (Huang et al 2004;Noble 2003). Third, schizophrenia is a complex disorder and its clinical heterogeneity may play a role in the outcomes of genetic association studies.…”

Section: Discussionmentioning

confidence: 99%

“…Each patient was examined initially by an experienced attending psychiatrist and was subsequently interviewed by a well-trained psychologist using the Chinese version of the modified Schedule for Affective Disorders and Schizophrenia-Lifetime Version (SADS-L) (Endicott and Spitzer 1978;Merikangas et al 1998). The interrater reliability κ values of the SADS-L were good-to-excellent for major depression, bipolar disorder, anxiety disorder, schizophrenia and substance abuse and dependence (Huang et al 2004). In addition, patients were classified into three homogeneous clinical subgroups: early-onset schizophrenia, late-onset schizophrenia and schizophrenia patients with a family history of schizophrenia.…”

Section: Sample Collectionmentioning

confidence: 99%

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Association study of catechol-O-methyltransferase gene polymorphisms with schizophrenia and psychopathological symptoms in Han Chinese

Chen¹,

Lu²,

Yeh³

et al. 2011

Genes, Brain and Behavior

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Although dysfunction of catechol-O-methyltransferase (COMT)-mediated dopamine transmission is implicatedin the etiology of schizophrenia, the human COMT gene has not been associated consistently with schizophrenia. The purpose of this study was to investigate whether the COMT gene is associated with the development of schizophrenia and whether the polymorphisms of this gene influence the psychopathological symptoms in patients with schizophrenia. Fourteen polymorphisms of the COMT gene were analyzed in a case-control study of 876 Han Chinese individuals (434 patients and 442 controls). All participants were screened using a Chinese version of the modified Schedule for Affective Disorders and Schizophrenia-Lifetime Version (SADS-L) and all patients met the criteria for schizophrenia. Furthermore, pretreatment of psychopathology was assessed using the Positive and Negative Syndrome Scale (PANSS) in a subset of 224 hospitalized schizophrenia patients, who were drugnaïve or drug-free, to examine the association between clinical symptomatology and COMT polymorphisms. No significant differences in allele or genotype frequencies were observed between schizophrenia patients and controls, for all variants investigated. Haplotype analysis showed that three haplotype blocks of the COMT gene were not associated with the development of schizophrenia. Moreover, these COMT polymorphisms did not influence the PANSS scores of schizophrenia patients. This study suggests that the COMT gene may not contribute to the risk of schizophrenia and to the psychopathological symptoms of schizophrenia among Han Chinese.

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Section: Discussionmentioning

confidence: 99%

Section: Sample Collectionmentioning

confidence: 99%

Association study of catechol-O-methyltransferase gene polymorphisms with schizophrenia and psychopathological symptoms in Han Chinese

Chen¹,

Lu²,

Yeh³

et al. 2011

Genes, Brain and Behavior

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show abstract

“…All participants were first interviewed by senior psychiatrists according to the diagnostic criteria of Diagnostic and Statistical Manual of Mental Disorders fourth edition (DSM-IV). The patients then received a structural interview conducted by clinical psychologist using the Chinese Version of the Modified Schedule of Affective Disorder and Schizophrenia-Life Time (SADS-L) 40 , which has good inter-rater reliability 41 . Patients diagnosed with other major mental illnesses, borderline personality disorder, substance abuse or dependence, and cognitive disorders other than BP-I or BP-II were excluded.…”

Section: Methodsmentioning

confidence: 99%

The Correlation between Plasma Brain-derived Neurotrophic Factor and Cognitive Function in Bipolar Disorder is Modulated by the BDNF Val66Met Polymorphism

Lee

2017

Eur. psychiatr.

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We explored the effect of the Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism (rs6265) on correlation between changes in plasma BDNF levels with cognitive function and quality of life (QoL) after 12 weeks of treatment in bipolar disorder (BD). Symptom severity and plasma BDNF levels were assessed upon recruitment and during weeks 1, 2, 4, 8 and 12. QoL, the Wisconsin Card Sorting Test (WCST), and the Conners' Continuous Performance Test (CPT) were assessed at baseline and endpoint. The BDNF Val66Met polymorphism was genotyped. Changes in cognitive function and QoL over 12 weeks were reduced using factor analysis for the evaluation of their correlations with changes in plasma BDNF. Five hundred forty-one BD patients were recruited and 65.6% of them completed the 12-week follow-up. Changes in plasma BDNF levels with factor 1 (WCST) were significantly negatively correlated (r = −0.25, p = 0.00037). After stratification of BD subtypes and BDNF genotypes, this correlation was significant only in BP-I and the Val/Met genotype (r = −0.54, p = 0.008). We concluded that changes in plasma BDNF levels significantly correlated with changes in WCST scores in BD and is moderated by the BDNF Val66Met polymorphism and the subtype of BD.Bipolar disorder (BD) is characterized by recurrent episodes of dysregulated moods 1,2 . With high heritability 3 , genetic factors had been regarded as an important etiology for BD. The most frequently seen subtypes of BD are bipolar I disorder (BP-I) and bipolar II disorder (BP-II). Being a chronic mental disorder, BD is increasingly regarded as a neurodegenerative disorder supported by imaging studies 4,5 . Brain-derived neurotrophic factor (BDNF) is an important protein for neuron development, growth and survival 6 . BDNF is robustly expressed

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“…Recently, particular attention has been paid to the decreased ALDH2 activity observed because of GTN tolerance. It is widely recognized that this enzyme strongly affects alcohol metabolism (Huang et al, 2004;Hendershot et al, 2009). Furthermore, ALDH2 plays a significant role in protecting cells from toxic substances (Klyosov et al, 1996;Wang et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Aldehyde dehydrogenase 2 protects human umbilical vein endothelial cells against oxidative damage and increases endothelial nitric oxide production to reverse nitroglycerin tolerance

Fang

Ma³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Medical nitroglycerin (glyceryl trinitrate, GTN) use is limited principally by tolerance typified by a decrease in nitric oxide (NO) produced by biotransformation. Such tolerance may lead to endothelial dysfunction by inducing oxidative stress. In vivo studies have demonstrated that aldehyde dehydrogenase 2 (ALDH2) plays important roles in GTN biotransformation and tolerance. Thus, modification of ALDH2 expression represents a potentially effective strategy to prevent and reverse GTN tolerance and endothelial dysfunction. In this study, a eukaryotic expression vector containing the ALDH2 gene was introduced into human umbilical vein endothelial cells (HUVECs) by liposome-mediated transfection. An indirect immunofluorescence assay showed that ALDH2 expression increased 24 h after transfection. Moreover, real-time polymerase chain reaction and western blotting revealed significantly higher ALDH2 mRNA and protein expression in the gene-transfected group than in the two control groups. GTN tolerance was induced by treating HUVECs with 10 mM GTN for 16 h + 10 min, which significantly decreased NO levels in control cells, but not in those transfected with ALDH2. Overexpression of ALDH2 increased cell survival against GTN-induced cytotoxicity and conferred protection from oxidative damage resulting from nitrate tolerance, accompanied by decreased production of intracellular reactive oxygen species and reduced expression of heme oxygenase 1. Furthermore, ALDH2 overexpression promoted Akt phosphorylation under GTN tolerance conditions. ALDH2 gene transfection can reverse and prevent tolerance to GTN through its bioactivation and protect against oxidative damage, preventing the development of endothelial dysfunction.

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Possible Interaction of Alcohol Dehydrogenase and Aldehyde Dehydrogenase Genes With the Dopamine D2 Receptor Gene in Anxiety‐Depressive Alcohol Dependence

Cited by 142 publications

References 109 publications

Association study of catechol-O-methyltransferase gene polymorphisms with schizophrenia and psychopathological symptoms in Han Chinese

Association study of catechol-O-methyltransferase gene polymorphisms with schizophrenia and psychopathological symptoms in Han Chinese

The Correlation between Plasma Brain-derived Neurotrophic Factor and Cognitive Function in Bipolar Disorder is Modulated by the BDNF Val66Met Polymorphism

Aldehyde dehydrogenase 2 protects human umbilical vein endothelial cells against oxidative damage and increases endothelial nitric oxide production to reverse nitroglycerin tolerance

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