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San Yuan Huang - One of the best experts on this subject based on the ideXlab platform.
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interaction between aldh2 1 1 and drd2 ankk1 taqi a1a1 genes may be associated with antisocial personality disorder not co morbid with Alcoholism
Addiction Biology, 2012Co-Authors: Jiafu Lee, San Yuan Huang, Sheng Yu Lee, Yun Hsuan Chang, Pohsiu Kuo, Shiou Lan Chen, Shih Heng Chen, Chun Hsien Chu, Weiwen LinAbstract:Previous studies on acetaldehyde dehydrogenase 2 (ALDH2) focused on drinking behavior or Alcoholism because the ALDH2*2 allele protects against the risk of developing Alcoholism. The mechanism provides that the ALDH2 gene's protective effect is also involved in dopamine metabolism. The interaction of the ALDH2 gene with neurotransmitters, such as dopamine, is suggested to be related to Alcoholism. Because Alcoholism is often co-morbid with antisocial personality disorder (ASPD), previous association studies on antisocial Alcoholism cannot differentiate whether those genes relate to ASPD with Alcoholism or ASPD only. This study examined the influence of the interaction effect of the ALDH2*1*1, *1*2 or *2*2 polymorphisms with the dopamine 2 receptor (DRD2) Taq I polymorphism on ASPD. Our 541 Han Chinese male participants were classified into three groups: antisocial Alcoholism (ASPD co-morbid with alcohol dependence, antisocial ALC; n = 133), ASPD without Alcoholism (ASPD not co-morbid with alcohol dependence, antisocial non-ALC; n = 164) and community controls (healthy volunteers from the community; n = 244). Compared with healthy controls, individuals with the DRD2 A1/A1 and the ALDH2*1/*1 genotypes were at a 5.39 times greater risk for antisocial non-ALC than were those with other genotypes. Our results suggest that the DRD2/ANKK1 and ALDH2 genes interacted in the antisocial non-ALC group; a connection neglected in previous studies caused by not separating antisocial ALC from ASPD. Our study made this distinction and showed that these two genes may be associated ASPD without co-morbid Alcoholism.
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interaction between serotonin transporter and serotonin receptor 1 b genes polymorphisms may be associated with antisocial Alcoholism
Behavioral and Brain Functions, 2012Co-Authors: Tzuyun Wang, San Yuan Huang, Sheng Yu Lee, Yun Hsuan Chang, Shiou Lan Chen, Shih Heng Chen, Chun Hsien Chu, Niansheng Tzeng, Chenlin Wang, Hui I LeeAbstract:Background: Several studies have hypothesized that genes regulating the components of the serotonin system, including serotonin transporter (5-HTTLPR) and serotonin 1 B receptor (5-HT1B), may be associated with Alcoholism, but their results are contradictory because of Alcoholism’s heterogeneity. Therefore, we examined whether the 5HTTLPR gene and 5-HT1B gene G861C polymorphism are susceptibility factors for a specific subtype of Alcoholism, antisocial Alcoholism in Han Chinese in Taiwan. Methods: We recruited 273 Han Chinese male inmates with antisocial personality disorder (ASPD) [antisocial Alcoholism (AS-ALC) group (n=120) and antisocial non-Alcoholism (AS-N-ALC) group (n=153)] and 191 healthy male controls from the community. Genotyping was done using PCR-RFLP. Results: There were no significant differences in the genotypic frequency of the 5-HT1B G861C polymorphism between the 3 groups. Although AS-ALC group members more frequently carried the 5-HTTLPR S/S, S/LG, and LG/LG genotypes than controls, the difference became non-significant after controlling for the covarying effects of age. However, the 5-HTTLPR S/S, S/LG, and LG/LG genotypes may have interacted with the 5-HT1B G861C C/C polymorphism and increased the risk of becoming antisocial Alcoholism. Conclusion: Our study suggests that neither the 5-HTTLPR gene nor the 5-HT1B G861C polymorphism alone is a risk factor for antisocial Alcoholism in Taiwan’s Han Chinese population, but that the interaction between both genes may increase susceptibility to antisocial Alcoholism.
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the relationship between serotonin receptor 1b polymorphisms a 161t and alcohol dependence
Alcoholism: Clinical and Experimental Research, 2009Co-Authors: San Yuan Huang, Shiou Lan Chen, Chenlin Wang, Pei Lin Wu, Jo Yung Wei Wu, Huei Chen Ko, Ru Band LuAbstract:Background: Several studies have suggested that the serotonin receptor 1B gene (5HT1B) may be important in the pathogenesis of alcohol dependence (Alcoholism; ALC; AD). We examined whether 5HT1B gene A-161T polymorphisms (rs130058) are a susceptibility factor for total AD and subgroups of AD. We further explored correlation of this 5HT1B gene variant between anxiety–depression Alcoholism (ANX/DEP ALC) and antisocial Alcoholism (antisocial ALC) subgroups because of the high comorbidity of anxiety–depression, antisocial personality disorder, and AD. Methods: We recruited 522 Han Chinese in Taiwan for this study: 322 AD patients and 200 controls. The patient group was recruited primarily from medical teaching hospitals; patients with antisocial Alcoholism were recruited from Taiwanese prisons. Individuals with AD were classified into 3 homogeneous clinical subgroups—pure Alcoholism (pure ALC), ANX/DEP ALC, and antisocial ALC—using DSM-IV diagnosis. The 5HT1B gene A-161T polymorphism was determined using PCR–RFLP. Results: No significant differences in genotypic and allelic frequencies were found between controls and the total AD group or between controls and the 3 AD subgroups. However, there were significant differences in the 5HT1B gene A-161T polymorphism at both the genotype and allelic levels between the ANX/DEP ALC and antisocial ALC subgroups. Conclusions: This study suggests that the 5HT1B gene A-161T polymorphism alone is not a risk factor for increasing susceptibility to either AD or its subtypes. However, 5HT1B gene A-161T polymorphisms might be one of the common genetic factors between the ANX/DEP ALC and antisocial ALC subgroups.
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the association between drd2 ankk1 5 httlpr gene and specific personality trait on antisocial Alcoholism among han chinese in taiwan
American Journal of Medical Genetics, 2008Co-Authors: Jiafu Lee, San Yuan HuangAbstract:Cloninger suggested that type II Alcoholism was associated with higher novelty seeking and less harm avoidance behaviors, which was similar to antisocial Alcoholism. Most previous studies have failed to recruit subjects that have antisocial personality disorder without Alcoholism due to the high coexisting likelihood of having antisocial personality disorder with Alcoholism in the majority of the examined populations. Thus, recruitment of individuals with antisocial non-Alcoholism (antisocial personality disorder) served as an important control group in examining Cloninger's hypothesis. Due to the documented protective effects against Alcoholism of ALDH2*1/*2 or *2/*2 genotype among the Han Chinese population, we recruited antisocial non-alcoholics from the Han Chinese population in Taiwan to verify Cloninger's hypotheses. A total of 127 Han Chinese subjects were recruited who met the diagnosis of antisocial Alcoholism (n = 43) or antisocial non-Alcoholism (n = 84). We found that the antisocial Alcoholism group scored higher on the novelty seeking behavior than did the antisocial non-Alcoholism group (t = 2.61, P = 0.01), but no difference was observed on the harm avoidance dimension between these two groups (t = 0.15, P = 0.88). In the novelty seeking scores, after stratification of DRD2 TaqI A genotypes, only a significant difference in 5-HTTLPR polymorphisms between antisocial alcoholics and antisocial non-alcoholics was found, indicating an interaction between DRD2 TaqI A1+ (include A1/A1 or A1/A2) and 5-HTTLPR S/S genotype (t = 2.75, P = 0.01) However, no significant difference was found in the harm avoidance personality trait between these two groups of Han Chinese in Taiwan. © 2007 Wiley-Liss, Inc.
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no Alcoholism protection effects of adh1b 2 allele in antisocial alcoholics among han chinese in taiwan
Alcoholism: Clinical and Experimental Research, 2005Co-Authors: Jiafu Lee, Weiwen Lin, San Yuan Huang, Tsojen Wang, Yuanhwa ChouAbstract:: Background: Thomasson et al., (1991) suggested that the genetic variation at ADH1B and ALDH2 influences the risk of Alcoholism. The ADH1B*2 and ALDH2*2 alleles had been thought to be protective against Alcoholism. Recent studies have suggested that either physiological tolerance of blood acetaldehyde, or innate insensitivity to it, or both may play a crucial role in keeping Alcoholism from developing by protecting against adverse reactions. ALDH inactive form resulting from ALDH2*2, which slows the elimination of acetaldehyde and the more active isozymes produced by ADH1B*2, could generate higher acetaldehyde levels and thus deter heavy drinking (Thomasson et al., 1991). The genotype frequency of ADH1B*2/*2 and ALDH2*(1/*2 or 2/*2), which are regarded protective against drinking behavior, is about 70% and 50%, respectively, among the Han Chinese population in Taiwan (Chen et al., 1999a). Most previous studies, however, have failed to separate the effects of antisocial personality disorder from those of Alcoholism because of their high comorbidity. To understand the relationship among Alcoholism, antisocial personality disorder, and the protective effects of ADH and ALDH, it is necessary to recruit individuals with antisocial personality disorder but without Alcoholism. This study was designed to stratify subjects by various ADH1B and ALDH2 genotypes for a more effective association study. The strata were: antisocial alcoholics, antisocial non-alcoholics, community alcoholics, and normal controls. Methods: We recruited 579 Han Chinese individuals in Taiwan, intending to examine the Alcoholism-protection effects of different ADH1B and ALDH2 genotypes with or without antisocial personality disorder. Results: We found no difference of ADH1B*2 allele frequency between the subjects of antisocial Alcoholism and subjects of antisocial non-Alcoholism, but we found significant difference of ALDH2*2 allele between these two groups. Conclusions: We concluded that there is no Alcoholism-protection effect of ADH1B*2 allele in antisocial alcoholics among Han Chinese in Taiwan.
Jiafu Lee - One of the best experts on this subject based on the ideXlab platform.
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interaction between aldh2 1 1 and drd2 ankk1 taqi a1a1 genes may be associated with antisocial personality disorder not co morbid with Alcoholism
Addiction Biology, 2012Co-Authors: Jiafu Lee, San Yuan Huang, Sheng Yu Lee, Yun Hsuan Chang, Pohsiu Kuo, Shiou Lan Chen, Shih Heng Chen, Chun Hsien Chu, Weiwen LinAbstract:Previous studies on acetaldehyde dehydrogenase 2 (ALDH2) focused on drinking behavior or Alcoholism because the ALDH2*2 allele protects against the risk of developing Alcoholism. The mechanism provides that the ALDH2 gene's protective effect is also involved in dopamine metabolism. The interaction of the ALDH2 gene with neurotransmitters, such as dopamine, is suggested to be related to Alcoholism. Because Alcoholism is often co-morbid with antisocial personality disorder (ASPD), previous association studies on antisocial Alcoholism cannot differentiate whether those genes relate to ASPD with Alcoholism or ASPD only. This study examined the influence of the interaction effect of the ALDH2*1*1, *1*2 or *2*2 polymorphisms with the dopamine 2 receptor (DRD2) Taq I polymorphism on ASPD. Our 541 Han Chinese male participants were classified into three groups: antisocial Alcoholism (ASPD co-morbid with alcohol dependence, antisocial ALC; n = 133), ASPD without Alcoholism (ASPD not co-morbid with alcohol dependence, antisocial non-ALC; n = 164) and community controls (healthy volunteers from the community; n = 244). Compared with healthy controls, individuals with the DRD2 A1/A1 and the ALDH2*1/*1 genotypes were at a 5.39 times greater risk for antisocial non-ALC than were those with other genotypes. Our results suggest that the DRD2/ANKK1 and ALDH2 genes interacted in the antisocial non-ALC group; a connection neglected in previous studies caused by not separating antisocial ALC from ASPD. Our study made this distinction and showed that these two genes may be associated ASPD without co-morbid Alcoholism.
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the association between drd2 ankk1 5 httlpr gene and specific personality trait on antisocial Alcoholism among han chinese in taiwan
American Journal of Medical Genetics, 2008Co-Authors: Jiafu Lee, San Yuan HuangAbstract:Cloninger suggested that type II Alcoholism was associated with higher novelty seeking and less harm avoidance behaviors, which was similar to antisocial Alcoholism. Most previous studies have failed to recruit subjects that have antisocial personality disorder without Alcoholism due to the high coexisting likelihood of having antisocial personality disorder with Alcoholism in the majority of the examined populations. Thus, recruitment of individuals with antisocial non-Alcoholism (antisocial personality disorder) served as an important control group in examining Cloninger's hypothesis. Due to the documented protective effects against Alcoholism of ALDH2*1/*2 or *2/*2 genotype among the Han Chinese population, we recruited antisocial non-alcoholics from the Han Chinese population in Taiwan to verify Cloninger's hypotheses. A total of 127 Han Chinese subjects were recruited who met the diagnosis of antisocial Alcoholism (n = 43) or antisocial non-Alcoholism (n = 84). We found that the antisocial Alcoholism group scored higher on the novelty seeking behavior than did the antisocial non-Alcoholism group (t = 2.61, P = 0.01), but no difference was observed on the harm avoidance dimension between these two groups (t = 0.15, P = 0.88). In the novelty seeking scores, after stratification of DRD2 TaqI A genotypes, only a significant difference in 5-HTTLPR polymorphisms between antisocial alcoholics and antisocial non-alcoholics was found, indicating an interaction between DRD2 TaqI A1+ (include A1/A1 or A1/A2) and 5-HTTLPR S/S genotype (t = 2.75, P = 0.01) However, no significant difference was found in the harm avoidance personality trait between these two groups of Han Chinese in Taiwan. © 2007 Wiley-Liss, Inc.
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no Alcoholism protection effects of adh1b 2 allele in antisocial alcoholics among han chinese in taiwan
Alcoholism: Clinical and Experimental Research, 2005Co-Authors: Jiafu Lee, Weiwen Lin, San Yuan Huang, Tsojen Wang, Yuanhwa ChouAbstract:: Background: Thomasson et al., (1991) suggested that the genetic variation at ADH1B and ALDH2 influences the risk of Alcoholism. The ADH1B*2 and ALDH2*2 alleles had been thought to be protective against Alcoholism. Recent studies have suggested that either physiological tolerance of blood acetaldehyde, or innate insensitivity to it, or both may play a crucial role in keeping Alcoholism from developing by protecting against adverse reactions. ALDH inactive form resulting from ALDH2*2, which slows the elimination of acetaldehyde and the more active isozymes produced by ADH1B*2, could generate higher acetaldehyde levels and thus deter heavy drinking (Thomasson et al., 1991). The genotype frequency of ADH1B*2/*2 and ALDH2*(1/*2 or 2/*2), which are regarded protective against drinking behavior, is about 70% and 50%, respectively, among the Han Chinese population in Taiwan (Chen et al., 1999a). Most previous studies, however, have failed to separate the effects of antisocial personality disorder from those of Alcoholism because of their high comorbidity. To understand the relationship among Alcoholism, antisocial personality disorder, and the protective effects of ADH and ALDH, it is necessary to recruit individuals with antisocial personality disorder but without Alcoholism. This study was designed to stratify subjects by various ADH1B and ALDH2 genotypes for a more effective association study. The strata were: antisocial alcoholics, antisocial non-alcoholics, community alcoholics, and normal controls. Methods: We recruited 579 Han Chinese individuals in Taiwan, intending to examine the Alcoholism-protection effects of different ADH1B and ALDH2 genotypes with or without antisocial personality disorder. Results: We found no difference of ADH1B*2 allele frequency between the subjects of antisocial Alcoholism and subjects of antisocial non-Alcoholism, but we found significant difference of ALDH2*2 allele between these two groups. Conclusions: We concluded that there is no Alcoholism-protection effect of ADH1B*2 allele in antisocial alcoholics among Han Chinese in Taiwan.
Adolf Pfefferbaum - One of the best experts on this subject based on the ideXlab platform.
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cognitive impairment severity in relation to signs of subclinical wernicke s encephalopathy in hiv and Alcoholism comorbidity
AIDS, 2020Co-Authors: Annepascale Le Berre, Adolf Pfefferbaum, Natalie M Zahr, Stephanie A Sassoon, Rosemary Fama, Edith V SullivanAbstract:Objectives The comorbidity of HIV infection and Alcoholism (ALC) is prevalent. Wernicke's encephalopathy, a neurological disorder resulting from thiamine depletion, has been generally associated with Alcoholism but has also been reported in HIV infection. This study examined whether subclinical Wernicke's encephalopathy signs could contribute to the heterogeneity of cognitive and motor deficits observed in individuals with both disease conditions (HIV+ALC). Design Sixty-one HIV+ALC individuals and 59 controls were assessed on attention and working memory, production, immediate and delayed episodic memory, visuospatial abilities, and upper limb motor function. Methods Using Caine criteria (dietary deficiency, oculomotor abnormality, cerebellar dysfunction, and altered mental state), HIV+ALC individuals were classified by subclinical Wernicke's encephalopathy risk factors. Results Signs of subclinical Wernicke's encephalopathy were present in 20% of the HIV+ALC participants. For attention/working memory, delayed memory, and upper limb motor function, HIV+ALC Caine 2+ (i.e. meeting two or three criteria) demonstrated the most severe deficits, scoring lower than HIV+ALC Caine 1 (i.e. meeting one criterion), HIV+ALC Caine 0 (i.e. meeting no criteria), and controls. Conclusion The high prevalence of subclinical signs of Wernicke's encephalopathy and relevance to performance indicate that this condition should be considered in assessment of HIV-infected individuals, especially when Alcoholism comorbidity is known or suspected. Above and beyond clinical factors, such as depression, Alcoholism and HIV disease-related variables, AIDS, hepatitis C and drug history known to mediate neuropsychological performance, subclinical Wernicke's encephalopathy signs could partly explain the heterogeneity in patterns and severity of cognitive and motor impairments in HIV-infected individuals with Alcoholism comorbidity.
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aberrant blood oxygen level dependent signal oscillations across frequency bands characterize the alcoholic brain
Addiction Biology, 2018Co-Authors: Juiyang Hong, Eva M Mulleroehring, Adolf Pfefferbaum, Edith V Sullivan, Dongjin Kwon, Tilman SchulteAbstract:Chronic Alcoholism is associated with widespread regional differences from controls in brain activity and connectivity dynamics measured by blood-oxygen-level-dependent (BOLD) signals. Identification of Alcoholism-related neurofunctional power dynamics using functional magnetic resonance imaging (fMRI) that relate to cognition and behavior may serve as biomarkers of Alcoholism. Previously, resting-state fMRI studies examined BOLD signals at a single low-frequency (LF) bandwidth. BOLD signals, however, oscillate systematically at different frequencies and are organized in a resting brain where LF oscillation facilitates long-distance communication between regions across cortical regions, whereas high-frequency (HF) oscillation occurs in closely localized, subcortical areas. Using a frequency power quantification approach, we investigated whether the organization of BOLD signal oscillations across all measured frequency bandwidths is altered in Alcoholism and relates to cognitive performance. Frequency-dependent oscillation power differences between 56 sober alcoholics and 56 healthy controls occurred for all frequency bands. Alcoholics exhibited greater frequency oscillation power in the orbitofrontal cortex and less power in the posterior insula within the HF bandwidth than controls. Aberrant orbitofrontal HF power was associated with poorer memory performance and slower psychomotor speed in alcoholics. Middle-frequency and LF power proved sensitive in detecting altered frequency oscillation dynamics in parietal and postcentral cortical regions of alcoholics. This study is novel in identifying alcohol-related differences in BOLD oscillation power of the full fMRI frequency bandwidth. Specifically, HF power aberrations were associated with poorer cognitive functioning in Alcoholism and may serve as a biomarker for identifying neural targets for repair.
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alcohol s effects on the brain neuroimaging results in humans and animal models
Alcohol research : current reviews, 2017Co-Authors: Natalie M Zahr, Adolf PfefferbaumAbstract:Brain imaging technology has allowed researchers to conduct rigorous studies of the dynamic course of Alcoholism through periods of drinking, sobriety, and relapse and to gain insights into the effects of chronic Alcoholism on the human brain. Magnetic resonance imaging (MRI) studies have distinguished alcohol-related brain effects that are permanent from those that are reversible with abstinence. In support of postmortem neuropathological studies showing degeneration of white matter, MRI studies have shown a specific vulnerability of white matter to chronic alcohol exposure. Such studies have demonstrated white-matter volume deficits as well as damage to selective gray-matter structures. Diffusion tensor imaging (DTI), by permitting microstructural characterization of white matter, has extended MRI findings in alcoholics. MR spectroscopy (MRS) allows quantification of several metabolites that shed light on brain biochemical alterations caused by Alcoholism. This article focuses on MRI, DTI, and MRS findings in neurological disorders that commonly co-occur with Alcoholism, including Wernicke's encephalopathy, Korsakoff's syndrome, and hepatic encephalopathy. Also reviewed are neuroimaging findings in animal models of Alcoholism and related neurological disorders. This report also suggests that the dynamic course of Alcoholism presents a unique opportunity to examine brain structural and functional repair and recovery.
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regional brain structural dysmorphology in human immunodeficiency virus infection effects of acquired immune deficiency syndrome Alcoholism and age
Biological Psychiatry, 2012Co-Authors: Adolf Pfefferbaum, Margaret J Rosenbloom, Torsten Rohlfing, Carol A Kemper, Stanley C Deresinski, Stephanie A Sassoon, Edith V SullivanAbstract:Background Human immunodeficiency virus (HIV) infection and Alcoholism each carries liability for disruption of brain structure and function integrity. Despite considerable prevalence of HIV-Alcoholism comorbidity, few studies examined the potentially heightened burden of disease comorbidity. Methods Participants were 342 men and women: 110 alcoholics, 59 with HIV infection, 65 with HIV infection and Alcoholism, and 108 healthy control subjects. This design enabled examination of independent and combined effects of HIV infection and Alcoholism along with other factors (acquired immune deficiency syndrome [AIDS]-defining events, hepatitis C infection, age) on regional brain volumes derived from T1-weighted magnetic resonance images. Results Brain volumes, expressed as Z scores corrected for intracranial volume and age, were measured in 20 tissue and 5 ventricular and sulcal regions. The most profound and consistent volume deficits occurred with alcohol use disorders, notable in the cortical mantle, insular and anterior cingulate cortices, thalamus, corpus callosum, and frontal sulci. The HIV-only group had smaller thalamic and larger frontal sulcal volumes than control subjects. HIV disease-related factors associated with greater volume abnormalities included CD4 cell count nadir, clinical staging, history of AIDS-defining events, infection age, and current age. Longer sobriety and less lifetime alcohol consumption were predictive of attenuated brain volume abnormalities in both alcohol groups. Conclusions Having HIV infection with Alcoholism and AIDS had an especially poor outcome on brain structures. That longer periods of sobriety and less lifetime alcohol consumption were predictive of attenuated brain volume abnormalities encourages the inclusion of alcohol recovery efforts in HIV/AIDS therapeutic settings.
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contribution of Alcoholism to brain dysmorphology in hiv infection effects on the ventricles and corpus callosum
NeuroImage, 2006Co-Authors: Adolf Pfefferbaum, Margaret J Rosenbloom, Torsten Rohlfing, Elfar Adalsteinsson, Carol A Kemper, Stanley C Deresinski, Edith V SullivanAbstract:Abstract Nonrigid registration and atlas-based parcellation methods were used to compare the volume of the ventricular system and the cross-sectional area of the midsagittal corpus callosum on brain MRIs from 272 subjects in four groups: patients with HIV infection, with and without Alcoholism comorbidity, alcoholics, and controls. Prior to testing group differences in regional brain metrics, each measure was corrected by regression analysis for significant correlations with supratentorial cranial volume and age, observed in 121 normal control men and women, whose age spanned six decades. Disregarding HIV disease severity, we observed a graded pattern of modest enlargement of the total ventricular system (0.28 SD for uncomplicated HIV, 0.65 SD for HIV comorbid with Alcoholism, and 0.72 SD for the Alcoholism group). The pattern of callosal thinning showed a similar but small (∼0.5 SD) graded effect. A different pattern emerged, however, when HIV severity in the context of Alcoholism comorbidity was factored into the analysis. Substantially greater volume abnormalities were present in individuals with a history of an AIDS-defining event or low CD4+ T cell counts (≤200 mm 3 ) irrespective of Alcoholism comorbidity, and the effect of HIV severity was disproportionately exacerbated by Alcoholism comorbidity, with 1 SD size deficit in the genu of corpus callosum and nearly 2 SD greater volume of the frontal and body regions of the ventricles for the AIDS + alcohol comorbid group. The differences in brain volumes between the AIDS groups with vs. without Alcoholism could not be attributed to differences in HIV disease severity, defined by CD4+ count, viral load, or Karnofsky score. The substantial effect of the Alcoholism–AIDS interaction on ventricular and callosal dysmorphology, in the context of the modest changes observed in non-AIDS, nonalcohol abusing HIV-infected individuals, highlight the need to consider alcohol use disorders as a major risk factor for neuropathology among HIV-infected persons.
Shiou Lan Chen - One of the best experts on this subject based on the ideXlab platform.
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interaction between aldh2 1 1 and drd2 ankk1 taqi a1a1 genes may be associated with antisocial personality disorder not co morbid with Alcoholism
Addiction Biology, 2012Co-Authors: Jiafu Lee, San Yuan Huang, Sheng Yu Lee, Yun Hsuan Chang, Pohsiu Kuo, Shiou Lan Chen, Shih Heng Chen, Chun Hsien Chu, Weiwen LinAbstract:Previous studies on acetaldehyde dehydrogenase 2 (ALDH2) focused on drinking behavior or Alcoholism because the ALDH2*2 allele protects against the risk of developing Alcoholism. The mechanism provides that the ALDH2 gene's protective effect is also involved in dopamine metabolism. The interaction of the ALDH2 gene with neurotransmitters, such as dopamine, is suggested to be related to Alcoholism. Because Alcoholism is often co-morbid with antisocial personality disorder (ASPD), previous association studies on antisocial Alcoholism cannot differentiate whether those genes relate to ASPD with Alcoholism or ASPD only. This study examined the influence of the interaction effect of the ALDH2*1*1, *1*2 or *2*2 polymorphisms with the dopamine 2 receptor (DRD2) Taq I polymorphism on ASPD. Our 541 Han Chinese male participants were classified into three groups: antisocial Alcoholism (ASPD co-morbid with alcohol dependence, antisocial ALC; n = 133), ASPD without Alcoholism (ASPD not co-morbid with alcohol dependence, antisocial non-ALC; n = 164) and community controls (healthy volunteers from the community; n = 244). Compared with healthy controls, individuals with the DRD2 A1/A1 and the ALDH2*1/*1 genotypes were at a 5.39 times greater risk for antisocial non-ALC than were those with other genotypes. Our results suggest that the DRD2/ANKK1 and ALDH2 genes interacted in the antisocial non-ALC group; a connection neglected in previous studies caused by not separating antisocial ALC from ASPD. Our study made this distinction and showed that these two genes may be associated ASPD without co-morbid Alcoholism.
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interaction between serotonin transporter and serotonin receptor 1 b genes polymorphisms may be associated with antisocial Alcoholism
Behavioral and Brain Functions, 2012Co-Authors: Tzuyun Wang, San Yuan Huang, Sheng Yu Lee, Yun Hsuan Chang, Shiou Lan Chen, Shih Heng Chen, Chun Hsien Chu, Niansheng Tzeng, Chenlin Wang, Hui I LeeAbstract:Background: Several studies have hypothesized that genes regulating the components of the serotonin system, including serotonin transporter (5-HTTLPR) and serotonin 1 B receptor (5-HT1B), may be associated with Alcoholism, but their results are contradictory because of Alcoholism’s heterogeneity. Therefore, we examined whether the 5HTTLPR gene and 5-HT1B gene G861C polymorphism are susceptibility factors for a specific subtype of Alcoholism, antisocial Alcoholism in Han Chinese in Taiwan. Methods: We recruited 273 Han Chinese male inmates with antisocial personality disorder (ASPD) [antisocial Alcoholism (AS-ALC) group (n=120) and antisocial non-Alcoholism (AS-N-ALC) group (n=153)] and 191 healthy male controls from the community. Genotyping was done using PCR-RFLP. Results: There were no significant differences in the genotypic frequency of the 5-HT1B G861C polymorphism between the 3 groups. Although AS-ALC group members more frequently carried the 5-HTTLPR S/S, S/LG, and LG/LG genotypes than controls, the difference became non-significant after controlling for the covarying effects of age. However, the 5-HTTLPR S/S, S/LG, and LG/LG genotypes may have interacted with the 5-HT1B G861C C/C polymorphism and increased the risk of becoming antisocial Alcoholism. Conclusion: Our study suggests that neither the 5-HTTLPR gene nor the 5-HT1B G861C polymorphism alone is a risk factor for antisocial Alcoholism in Taiwan’s Han Chinese population, but that the interaction between both genes may increase susceptibility to antisocial Alcoholism.
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the relationship between serotonin receptor 1b polymorphisms a 161t and alcohol dependence
Alcoholism: Clinical and Experimental Research, 2009Co-Authors: San Yuan Huang, Shiou Lan Chen, Chenlin Wang, Pei Lin Wu, Jo Yung Wei Wu, Huei Chen Ko, Ru Band LuAbstract:Background: Several studies have suggested that the serotonin receptor 1B gene (5HT1B) may be important in the pathogenesis of alcohol dependence (Alcoholism; ALC; AD). We examined whether 5HT1B gene A-161T polymorphisms (rs130058) are a susceptibility factor for total AD and subgroups of AD. We further explored correlation of this 5HT1B gene variant between anxiety–depression Alcoholism (ANX/DEP ALC) and antisocial Alcoholism (antisocial ALC) subgroups because of the high comorbidity of anxiety–depression, antisocial personality disorder, and AD. Methods: We recruited 522 Han Chinese in Taiwan for this study: 322 AD patients and 200 controls. The patient group was recruited primarily from medical teaching hospitals; patients with antisocial Alcoholism were recruited from Taiwanese prisons. Individuals with AD were classified into 3 homogeneous clinical subgroups—pure Alcoholism (pure ALC), ANX/DEP ALC, and antisocial ALC—using DSM-IV diagnosis. The 5HT1B gene A-161T polymorphism was determined using PCR–RFLP. Results: No significant differences in genotypic and allelic frequencies were found between controls and the total AD group or between controls and the 3 AD subgroups. However, there were significant differences in the 5HT1B gene A-161T polymorphism at both the genotype and allelic levels between the ANX/DEP ALC and antisocial ALC subgroups. Conclusions: This study suggests that the 5HT1B gene A-161T polymorphism alone is not a risk factor for increasing susceptibility to either AD or its subtypes. However, 5HT1B gene A-161T polymorphisms might be one of the common genetic factors between the ANX/DEP ALC and antisocial ALC subgroups.
Giiasheun Peng - One of the best experts on this subject based on the ideXlab platform.
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effect of the allelic variants of aldehyde dehydrogenase aldh2 2 and alcohol dehydrogenase adh1b 2 on blood acetaldehyde concentrations
Human Genomics, 2009Co-Authors: Giiasheun PengAbstract:Alcoholism is a complex behavioural disorder. Molecular genetics studies have identified numerous candidate genes associated with Alcoholism. It is crucial to verify the disease susceptibility genes by correlating the pinpointed allelic variations to the causal phenotypes. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are the principal enzymes responsible for ethanol metabolism in humans. Both ADH and ALDH exhibit functional polymorphisms among racial populations; these polymorphisms have been shown to be the important genetic determinants in ethanol metabolism and Alcoholism. Here, we briefly review recent advances in genomic studies of human ADH/ALDH families and Alcoholism, with an emphasis on the pharmacogenetic consequences of venous blood acetaldehyde in the different ALDH2 genotypes following the intake of various doses of ethanol. This paper illustrates a paradigmatic example of phenotypic verifications in a protective disease gene for substance abuse.
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pharmacokinetic and pharmacodynamic basis for partial protection against Alcoholism in asians heterozygous for the variant aldh2 2 gene allele
Pharmacogenetics and Genomics, 2007Co-Authors: Giiasheun Peng, Yichyan Chen, Tienping Tsao, Mingfang Wang, Shihjiun YinAbstract:ObjectivesIt has been well documented that although homozygosity of the variant aldehyde dehydrogenase-2 (ALDH2) gene allele, ALDH2*2, in Asians almost fully protects against Alcoholism, the heterozygosity only affords a partial protection to varying degrees. The full protection against Alcoholism h