Alcoholism Thesis Paper

Alcoholism Thesis Paper-4
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.

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.

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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].

The activated form of acetate, acetyl-Co A, can be metabolized into ketone bodies, fatty acids, amino acids and steroids, in addition to oxidation in the Krebs cycle.

Cytochrome P450s (for example, those encoded by the gene CYP2E1) and catalase also metabolize a small fraction of ingested ethanol.

Human genetic studies on alcohol-related phenotypes have used family-based linkage and population-based association analyses to identify quantitative trait loci (QTLs).

Linkage studies are based on co-segregation between genetic markers and alcohol dependence in families with several affected members.The term 'alcoholism' was first coined by Magnus Huss to describe the persistence of drinking despite adverse health effects.The Diagnostic and Statistical Manual of Mental Disorders classifies alcoholism as an addictive disorder [1].The main pathway of ethanol metabolism involves its conversion to acetaldehyde by alcohol dehydrogenase (ADH; Figure 1).Acetaldehyde is oxidized to acetate by aldehyde dehydrogenase (ALDH).In both designs, large numbers of individuals are required to detect QTLs with small effects.Early efforts to dissect the genetic basis of alcohol consumption and addiction in humans were based on candidate genes.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.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.

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