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<p>Parkinson’s Disease (PD) and Alcohol Use Disorder (AUD) are neurodegenerative conditions that involve similar neurobiological pathways and affect motivation and reward dysregulations. This project aims to explore whether PD-related insults affect alcohol-related motivation and reward. We utilized paraquat (PQ) exposure as a neurotoxicant-induced model for PD and mice selectively bred for a differential in alcohol preference as a model for genetic and neurobiological susceptibility for high/low alcohol consumption. In Experiment 1, binge-like alcohol drinking after three weeks of PQ exposure (10 mg/kg, i.p. once per week) or saline was assessed in HAP male and female mice. The four-day Drinking in the Dark (DID) procedure was used to induce binge-like alcohol drinking. Dorsal (DS) and ventral (VS) striatal catecholamines were analyzed after DID. Overall, PQ-treated HAP males had significantly lower alcohol intake than saline-treated males. This effect was absent in female HAP mice. Catecholamine quantification showed lower DOPAC levels in VS of PQ-treated vs. saline-treated HAP male mice. Experiment 2 assessed alcohol-induced locomotor sensitization in adult male and female high (HAP) and low-alcohol-preferring (LAP) mice after PQ exposure. Following the same 3 weeks of PQ or saline exposure, mice received 6 sensitization induction days with either 3 g/kg i.p. EtOH or saline. On test day, an alcohol challenge dose of 2 g/kg in all mice was used to determine the expression of locomotor sensitization. PQ exposure had no significant effect on locomotor activity and sensitization. However, PQ-treated mice showed great variability in their alcohol-induced locomotor activity compared to other groups. These data suggest a sex difference in PQ’s effect on alcohol binge-like drinking. However, PQ’s effect on alcohol-induced locomotor sensitization is not conclusive. This project will elucidate potential mechanisms behind PD-related neuropsychiatric comorbid conditions like AUD. Such findings may assist in early diagnosis and treatment refinement, as these comorbidities precede the motor manifestation of PD by decades and significantly impact the quality of life.</p>

Background. Alcohol-use is an identifiable and preventable risk factor among women seeking to become pregnant. Maternal alcohol-use during pregnancy may be related to congenital cardiac defects, one of the leading types of birth defects. Methods. This study used data from the Pregnancy Risk Assessment Monitoring Surveillance (PRAMS), an ongoing national study administered in selected participating states. Alcohol use and other risk factors were obtained from the PRAMS survey linked to birth defects data from birth certificates in 9 participating states over a ten year period (1996-2005). In this study cases included infants born with a congenital cardiac defect as indicated on the birth certificate. Cases were compared to two control groups. One control group consisted of infants with no indication of a congenital abnormality on their birth certificate. A second control group consisted of infants born with Down's syndrome indicated on their birth certificate. Odds ratios for congenital cardiac defects were computed for maternal alcohol use, frequent drinking, binge drinking and continued drinking through logistic regression. Results. Differences were found in the odds of congenital cardiac defects among mothers who reported binge drinking on more than once occasion in the 3 months prior to pregnancy. Maternal binge drinking on multiple occasions was found to be a risk factor for congenital cardiac defects (OR 2.99; CI 1.19-7.51) when nonaffected controls were used as a reference group. Significant interaction between binge drinking and smoking in the 3 months prior to pregnancy was noted with both control groups. Conclusion. Binge drinking in early pregnancy may be a risk factor for congenital cardiac defects, particularly when combined with smoking. / Public Health