Presenter:
Khamani Ridley
Cannabis is the most commonly used illicit drug in the United States, with 3 in 10 cannabis users developing cannabis use disorder (CUD). Increased legalization of cannabis for medical and recreational purposes has contributed to a rise in use. Many individuals use cannabis due to its mood-enhancing effects, but misconceptions about its addictive qualities, potential withdrawal symptoms, and long-term health consequences highlight a need for further research. In particular, there is limited information on which specific factors of cannabis use relate to Quality of Life (QoL), a subjective concept that measures individuals' satisfaction. Understanding this relationship is critical in developing treatments targeting cannabis users' mental health and well-being. This project aims to identify baseline cannabis use factors related to QoL in individuals with cannabis use disorder. We explored several variables to examine their relationship with patients' Quality of Life scores. Data was analyzed from double-blind, randomized controlled trial with a sample of 20 treatment-seeking individuals with CUD. Spearman's Rank-Order Correlations were run between participants' raw scores on the Quality of Life, Enjoyment, and Satisfaction Questionnaire Short Form (Q-LES-Q-SF) and the Pittsburgh Sleep Quality Index (PSQI), Marijuana Problem Scale (MPS), Quick Inventory of Depressive Symptomatology (QIDS), and Generalized Anxiety Disorder-7 (GAD-7) at baseline. Independent Samples t-tests were run to assess differences in QoL, Age of Onset, and Age of Regular Use between median-split age groups. No statistically significant correlations were found. QoL did not differ by Age of Regular use (t(18) = 1.373, p = .186), but the effect size (Cohen's d = .614) indicates potential clinical significance. Quality of Life as an outcome measure for cannabis use disorder requires further exploration with larger sample sizes. Prospective studies, with self-reports conducted at multiple timepoints, are needed to determine a causal relationship between cannabis use and Quality of Life. Adolescent Binge Drinking Causes Persistent Alterations in Hippocampal Astroglial Morphology: Extending to Hilus
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Presenter: Khamani Ridley
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Approximately 3.3 million individuals aged 12 to 20 report binge drinking in the past month, which is associated with greater risk for lifetime alcohol use disorders (AUD) and alterations in learning and memory. Adolescent intermittent ethanol (AIE), a rodent model of binge drinking, has been found to persistently alter hippocampal structure and function, a region important in memory and cognition. AIE alters dorsal hippocampal neuroinflammation and neurodegeneration. Non-neuronal astrocytes exist in a proinflammatory state and make less connectivity with excitatory synapses. In this proinflammatory state, astrocytes increase expression of an intermediate filament called glial fibrillary acidic protein (GFAP). Proinflammatory astrocytes result in neuronal damage and impairments in memory, which is associated with neurodegenerative diseases. Prior studies show that, in adulthood following AIE exposure, dorsal hippocampal (dHPC) CA1 astrocytes exhibit a proinflammatory state in both sexes, with an enlarged soma, increased branching, and shortened processes. This suggests that other areas of the trisynaptic dHPC, such as the Hilar region which integrates cholinergic input from the basal forebrain, may be altered as well. In this study, 16 male and female Sprague Dawley rats (Charles River, Raleigh, NC) underwent AIE given 10 doses (Decon Labs, Prussia, PA, US; 5g/kg, i.g., 35% EtOH) with a schedule of two days on, one day off, and two days off in adolescence (PND 31-46). In adulthood (PND 77), rat brains were harvested for immunohistochemistry, where they were stained for GFAP expression. Astrocytes in the Hilar dHPC were visualized with a Brightfield microscope and Neurolucida (MBF Bioscience, Williston, VT, USA). The study was used to trace astrocytes to create 3D reconstructions to analyze process length, branching, and Sholl complexity. If a history of AIE creates proinflammatory astrocytes in the Hilar dHPC, it may indicate dysregulation of the trisynaptic circuit, which is integral for memory formation and maintenance.
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Duke University / 2025
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Presenter: Khamani Ridley