Publication Date
Fall 2026
College
College of Natural Resources & Sciences
Department
Mathematics & Data Science
Document Type
Poster
Description
Microglia are immune cells in the brain that switch phenotypes to maintain neural health, but disruptions in this regulation may contribute to Alzheimer’s Disease (AD). We developed an agent-based model to link cell mechanisms to tissue-level patterns, incorporating both individual cell responses to localized signaling and the effects of APOE and TREM2 variants on microglial metabolism and clearance. Through computational experiments, we simulate how impaired lipid clearance and sensing lead to a pro-inflammatory microglial population and chronic inflammation. Our framework offers insight into how local dysfunction progresses to persistent neuroinflammation and promotes conditions like AD.