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Alcohol-related brain damage [1] [2] alters both the structure and function of the brain as a result of the direct neurotoxic effects of alcohol intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the frontal lobe , [ 3 ] limbic system , and cerebellum , [ 4 ] with widespread ...
Alcohol acts as a general central nervous system depressant, but it also affects some specific areas of the brain to a greater extent than others. Memory impairment caused by alcohol has been linked to the disruption of hippocampal function—particularly affecting gamma-Aminobutyric acid (GABA) and N-methyl-D-aspartate (NMDA) neurotransmission which negatively impacts long-term potentiation ...
Alcohol is a tiny molecule, bathing nearly every cell in the body when we drink. The basic trajectory of liquor in the body is from a person's mouth, through the esophagus, to the stomach ...
The reinforcing effects of alcohol consumption are mediated by acetaldehyde generated by catalase and other oxidizing enzymes such as cytochrome P-4502E1 in the brain. [60] Although acetaldehyde has been associated with some of the adverse and toxic effects of ethanol, it appears to play a central role in the activation of the mesolimbic ...
The deformed brain is a preserved specimen estimated to be more than 2,000 years old. There's no evidence it's appearance is related to alcohol use. Image showing purported effects of alcohol is ...
The cited allergic reaction-like symptoms: (a) do not appear due to classical IgE or T cell-related allergen-induced reactions but rather the actions of acetaldehyde in stimulating the release of histamine, a probable mediating cause of these symptoms; (b) typically occur within 30–60 minutes of ingesting alcoholic beverages; and (c) occur in ...
Alcohol has a powerful effect on glutamate as well. Alcohol decreases glutamate's ability to bind with NMDA and acts as an antagonist of the NMDA receptor, which plays a critical role in LTP by allowing Ca2+ to enter the cell. These inhibitory effects are thought to be responsible for the "memory blanks" that can occur at levels as low as 0.03% ...
Chronic alcohol exposure decreases the number of proliferating cells that are radial glia-like, preneuronal, and intermediate types, while not affecting early neuronal type cells; suggesting ethanol treatment alters the precursor cell pool. Furthermore, there is a greater decrease in differentiation and immature neurons than there is in ...