ETHYL ALCOHOL METABOLISM AND NEUROBIOLOGY IN HUMANS: FACTORS CONTRIBUTING TO ALCOHOLISM AND NEUROTOXICITY
Open Access
Author:
Arnold, Josh
Area of Honors:
Biology
Degree:
Bachelor of Science
Document Type:
Thesis
Thesis Supervisors:
Dr. James Harold Marden, Thesis Supervisor Dr. James Harold Marden, Thesis Supervisor Dr. James Harold Marden, Thesis Honors Advisor Dr. David Peter Hughes, Faculty Reader
The consumption of ethanol has profound effects on human metabolism and central nervous system function. The oxidation of ethanol by alcohol dehydrogenase results in the production of toxic acetaldehyde and excess NADH, causing the disruption of normal metabolic processes and organ function. The risk for tissue damage and alcoholism is influenced by genetic polymorphisms in alcohol dehydrogenase and acetaldehyde dehydrogenase. Ethanol modulates the release of most major neurotransmitters in the brain including GABA, acetylcholine, glutamate, dopamine, serotonin, and opioid peptides. Changes in neurotransmission produce ethanol’s characteristic psychoactive properties. Genetic variation in neurotransmitter receptors is correlated with susceptibility to the effects of alcohol and the risk of alcoholism. With chronic consumption, ethanol can cause irreversible brain damage through thiamine depletion and glutamate excitotoxicity. Ideas for further research are proposed.
