Polymorphism of Tumor Necrosis Factor‐β and Alcohol Dehydrogenase Genes and Alcoholic Brain Atrophy in Japanese Patients

Yamaguchi, Masayoshi; Takamatsu, Masashi; Maezawa, Yoshihiko; Takagi, Masaru; Araki, Takashi; Satoh, Shunnya; Toda, Gotaro; Sakai, Saburo

doi:10.1111/j.1530-0277.2001.tb02409.x

Cited by 4 publications

(1 citation statement)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Many regions that are normal in uncomplicated alcoholics are damaged in those with Wernicke-Korsakoff syndrome. 1022 The apolipoprotein Eε 4 (APOEε 4) allele was reportedly more prevalent in alcoholic Wernicke-Korsakoff patients with "global" intellectual impairment than in those with a more purely amnestic disorder. 1014 In an autopsy study using nonalcoholic controls, selective neuronal loss in the superior frontal association cortex of chronic alcoholics with or without prior evidence of Wernicke-Korsakoff syndrome appeared to be confined to non-GABAergic pyramidal neurons.…”

Section: Observations In Humansmentioning

confidence: 99%

Ethanol

Brust

2004

Neurological Aspects of Substance Abuse

View full text Add to dashboard Cite

Section: Observations In Humansmentioning

confidence: 99%

Ethanol

Brust

2004

Neurological Aspects of Substance Abuse

View full text Add to dashboard Cite

Interaction between alcohol dehydrogenase II gene, alcohol consumption, and risk for breast cancer

et al. 2002

View full text Add to dashboard Cite

MaeIII Restriction Fragment Length Polymorphism in exon 3 of the alcohol dehydrogenase II was assessed in serum from 467 randomly selected German women and 278 women with invasive breast cancer to evaluate the interaction between a polymorphism of the alcohol dehydrogenase II gene, alcohol consumption and risk for breast cancer. In both groups, usual consumption of different alcoholic beverages was asked for using semiquantitative food frequency questionnaires. We used multivariable logistic regression to separately estimate the association between alcohol consumption and alcohol dehydrogenase II polymorphism in the population sample and women with breast cancer. The alcohol dehydrogenase II polymorphism was detected in 14 women from the population sample (3.0%) and in 27 women with invasive breast cancer (9.7%). Frequency of alcohol consumption was independent of the genotype in the population sample. In women with breast cancer, there was a significant inverse association between the alcohol dehydrogenase II polymorphism and frequency of alcohol consumption (adjusted case-only odds ratio over increasing frequency of alcohol consumption=0.5; P for interaction=0.02). We observed a gene-environment interaction between the alcohol dehydrogenase II polymorphism, alcohol consumption, and risk for breast cancer. Breast cancer risk associated with alcohol consumption may vary according to the alcohol dehydrogenase II polymorphism, probably due to differences in alcohol metabolism. British Journal of Cancer (2002) (Longnecker, 1994;Smith-Warner et al, 1998;Singletary and Gapstur, 2001;Willett, 2001). Despite growing interest in genetic polymorphisms of the enzymes involved in alcohol metabolism for several diseases associated with alcohol comsumption (Hines et al, 2001;McCarver, 2001; Yamauchi et al, 2001a,b), data regarding the role of these polymorphisms as to the risk for breast cancer are sparse (Freudenheim et al, 1999;Hines et al, 2000). These polymorphisms are good candidates for gene-environment interactions (Millikan et al, 1995), however, because they are likely to influence the most plausible biologic mechanism linking alcohol consumption to risk for breast cancer, i.e. endogenous oestrogens.In humans, alcohol is almost entirely metabolised by oxidative detoxification, mainly dependent on two enzymes, class I alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). Both enzymes exhibit genetic polymorphisms influencing the rate of conversion from alcohol to acetaldehyde and to acetate (Smith, 1986). The class I ADH isoenzymes are formed by dimeric associations of a, b, and g subunits controlled by three separate gene loci ADH1, ADH2, and ADH3, respectively (Agarwal and Goedde, 1990). Despite recent reports regarding the ADH3 polymorphism and risk for breast cancer (Freudenheim et al, 1999;Hines et al, 2000), nothing is known about the role of the less frequent but metabolically more relevant ADH2 polymorphism and its interaction with alcohol consumption for the risk of breast cancer.The aim of the ...

show abstract

Tumour Necrosis Factor in Neuroplasticity, Neurogenesis and Alcohol Use Disorder

Cooper

Beecher

Chehrehasa

et al. 2020

BPL

View full text Add to dashboard Cite

Alcohol use disorder is a pervasive and detrimental condition that involves changes in neuroplasticity and neurogenesis. Alcohol activates the neuroimmune system and alters the inflammatory status of the brain. Tumour necrosis factor (TNF) is a well characterised neuroimmune signal but its involvement in alcohol use disorder is unknown. In this review, we discuss the variable findings of TNF's effect on neuroplasticity and neurogenesis. Acute ethanol exposure reduces TNF release while chronic alcohol intake generally increases TNF levels. Evidence suggests TNF potentiates excitatory transmission, promotes anxiety during alcohol withdrawal and is involved in drug use in rodents. An association between craving for alcohol and TNF is apparent during withdrawal in humans. While anti-inflammatory therapies show efficacy in reversing neurogenic deficit after alcohol exposure, there is no evidence for TNF's essential involvement in alcohol's effect on neurogenesis. Overall, defining TNF's role in alcohol use disorder is complicated by poor understanding of its variable effects on synaptic transmission and neurogenesis. While TNF may be of relevance during withdrawal, the neuroimmune system likely acts through a larger group of inflammatory cytokines to alter neuroplasticity and neurogenesis. Understanding the individual relevance of TNF in alcohol use disorder awaits a more comprehensive understanding of TNF's effects within the brain.

show abstract

Polymorphism of Tumor Necrosis Factor‐β and Alcohol Dehydrogenase Genes and Alcoholic Brain Atrophy in Japanese Patients

Cited by 4 publications

References 28 publications

Ethanol

Ethanol

Interaction between alcohol dehydrogenase II gene, alcohol consumption, and risk for breast cancer

Tumour Necrosis Factor in Neuroplasticity, Neurogenesis and Alcohol Use Disorder

Contact Info

Product

Resources

About