Alcoholism Thesis Paper

Alcoholism Thesis Paper-64
ADH1B, ALDH2 and ADH4 influence alcohol consumption and have been implicated as risk factors for developing alcohol abuse or dependence [9–11]. Ethanol is converted to acetaldehyde by alcohol dehydrogenase (ADH) and subsequently to acetate by aldehyde dehydrogenase (ALDH).

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By contrast, association studies evaluate the strength of association between genetic variants and alcohol phenotypes in samples of unrelated individuals; these can be attributable to a causal effect of the variant or linkage disequilibrium (LD) between the molecular variant and the true causal allele.

Association analyses give more precise localization of QTLs than linkage studies; however, false-positive associations can arise from population stratification of cases and controls, and by chance in small samples.

This pathway is indirectly activated by alcohol through the release of other neurotransmitters, including acetylcholine, dopamine, glutamate, gamma-aminobutyric acid (GABA), opioids and serotonin.

Several candidate genes in neurotransmitter pathways associated with the ventral tegmental area and nucleus accumbens have been associated with alcohol dependence, including the genes encoding cholinergic receptor, muscarinic 2 (CHRM2) [12]; cholinergic receptor, nicotinic, alpha 5 (CHRNA5) [13]; catechol-O-methyltransferase (COMT) [9]; GABA A receptor, alpha 2 (GABRA2) [14]; glutamate receptor, metabotropic 8 (GRM8) [15]; solute carrier family 6 (neurotransmitter transporter, serotonin), member 4 (5-HTT) [16]; nuclear factor of kappa light polypeptide gene enhancer in B cells 1 (NFKB1) [17]; monoamine oxidase A (MAOA) [18]; neuropeptide Y receptor Y2 (NPY2R) [19]; opioid receptor, kappa 1 (OPRK1) [20]; opioid receptor, mu 1 (OPRM1) [21]; prodynorphin (PDYN) [20]; and tachykinin receptor 3 (TACR3) [22].

In addition, a small fraction of ethanol is metabolized by cytochrome P450 2E1 (CYP2E1) and in the brain by catalase.

The diagram presents only those members of the ADH and ALDH families referred to in the text.The risk of upper gastrointestinal cancer is increased by a missense variant in the gene encoding aldehyde dehydrogenase (ALDH), which is found in some 500 million East Asians [2].Depression, epilepsy, hypertension and hemorrhagic stroke occur secondary to alcohol consumption [3].It is a complex disorder affected by genetic, epigenetic and environmental etiologic factors.High levels of alcohol intake are associated with impairment of multiple organs, including brain, liver, pancreas and the immune system.Finally, alcohol consumption during pregnancy can result in birth defects that comprise fetal alcohol syndrome [4].The diversity of pathologic effects of alcohol indicates that this drug exerts toxicity through multiple mechanisms, each of which can be modulated by different genetic variants.Accumulation of acetaldehyde is responsible for the physiological malaise commonly known as 'hangover'.The positive reinforcing effects of alcohol are mediated through the corticomesolimbic dopaminergic reward pathway, which extends from the ventral tegmental area to the nucleus accumbens and is modulated by a wide range of neurotransmitters.This can be done by considering the effects of molecular polymorphisms on phenotypes mediated via complex networks of transcriptional, protein, metabolic and neurogenetic endophenotypes.Here, we review genetic risk factors and transcriptional correlates for alcohol consumption in humans, with insights from studies on model genetic organisms.


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