Project Type
Poster
Publication Date
Spring 5-2-2025
Department or Program
Biological Sciences
College
College of Arts & Sciences
Faculty Mentor #1
Dr. Deborah O’Dell
Abstract
Neuroinflammation, driven by proinflammatory cytokines, is linked to Alzheimer’s Disease (AD). Norepinephrine (NE) activates microglial adrenergic receptors, potentially increasing IL-1β production. This study investigates the effects of NE exposure on IL-1β production in human microglial cells, using adrenergic receptor-specific antagonists to isolate the effects of α1-AR, α2-AR, β2-AR, and combined α1& β2 -AR pathways. Microglia were treated with 100nM antagonists and exposed to control (0μM), medium (1 μM) or high (10 μM) NE concentrations. Media was collected at 3, 6 and 9 days, and protein content was standardized using a BioRad Protein Assay. IL-1β levels were quantified via ELISA (Sigma). In general, high NE treatments resulted in higher levels of IL-1β with active β adrenergic receptors resulting in the highest levels. The lowest levels of IL-1β were seen when both the α1 and β adrenergic receptors were blocked. Active α2 receptors were associated with lower IL-1β production. These findings highlight the role of adrenergic receptor pathways in modulating IL-1β production and suggest that targeting specific adrenergic receptors may provide therapeutic strategies to mitigate stress-induced neuroinflammation and slow Alzheimer’s disease progression.