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A ‘binge’ corresponds to consuming 5 or more (males) or 4 or more (females) drinks within 2 hours. Forty percent of college students binge drink at least once a month, and 17% five or more times a month. The Panhandle-South Plains region has the highest past month binge drinking rate in Texas (27% of general population 12 years and older). Clinical and basic science evidence suggests adolescents and young adult brains may be especially susceptible to alcohol-induced injury. Our working hypothesis is each occasion of binge drinking represents a neurological insult with severity of damage and cognitive dysfunction a function of the duration and intensity of this behavior. Specifically, this study will examine how neurological, biochemical, and cognitive impacts of binge alcohol consumption vary with duration and intensity of binging in both a rat model and college-aged human participants.
Specific Aim I: Examine the neuropathological sequelae of binge drinking.
1. Test the hypothesis serum levels of S100B (protein marker of brain damage) and homocysteine (HCY; amino acid related to neuropathology and cognitive decline) increase in proportion to duration, intensity, and/or recency of binge alcohol consumption in both a rat model and humans.
2. Test the hypothesis increased serum S100B and HCY levels following binge alcohol exposure reflect increased CNS release by comparing serum to CSF levels in rats.
3. Test the hypothesis binge alcohol consumption is related to histological neuropathology in the hippocampus and parahippocampal, prefrontal, and anterior cingulate cortices in rats. Test the hypothesis that morphometric MRI measures of these regions in humans will differ between nonbingingparticipants and those with the longest duration or most intense binge drinking.
Specific Aim II: Examine the cognitive functioning sequelae of binge drinking.
1. Test the hypothesis decreased performance in memory and executive functioning are proportionate to duration, intensity, and/or recency of binge alcohol consumption in humans and rats.
2. Use functional MRI to test the hypothesis that duration, intensity, and/or recency of binge drinking are related to reduced and/or altered patterns of brain activity during performance of executive functioning cognitive tasks.
3. Test the hypothesis that increased S100B and/or HCY serum levels are related to decreased cognitive performance in both rats and humans.
4. Test the hypothesis that binge induced hippocampus and parahippocampal neuropathology in rats is related to decreased memory performance. Test the hypothesis that binge induced prefrontal and anterior cingulate neuropathology in rats is related to decrease in working memory and executive function.