BME PhD Defense Announcement for Jee Hyun Park (D. Brubaker and D. Chan, co-advisors) Everyone is invited to attend the public presentation beginning at 9:30 AM ET. Title: Cross-Species Modeling of Therapeutic Signatures in Alzheimer's Disease Date: September 16, 2025 Time: 9:30 AM ET Location: MJIS 2001 and Zoom - https://purdue-edu.zoom.us/j/98861664455?pwd=yOMFyxBWuk4QYPFr4hEjPQmNeJnCrm.1<https://nam04.safelinks.protection.outlook.com/?url=https%3A%2F%2Fpurdue-edu.zoom.us%2Fj%2F98861664455%3Fpwd%3DyOMFyxBWuk4QYPFr4hEjPQmNeJnCrm.1&data=05%7C02%7Cbmegradstudents-list%40ecn.purdue.edu%7C79a6bb7effac42ef442508ddefbc8153%7C4130bd397c53419cb1e58758d6d63f21%7C1%7C0%7C638930315097438517%7CUnknown%7CTWFpbGZsb3d8eyJFbXB0eU1hcGkiOnRydWUsIlYiOiIwLjAuMDAwMCIsIlAiOiJXaW4zMiIsIkFOIjoiTWFpbCIsIldUIjoyfQ%3D%3D%7C0%7C%7C%7C&sdata=bFQg0efd3%2BNpzLto%2Bf8Awr2xrBwucPX9VZEzUb6Dld4%3D&reserved=0> Committee: Dr. Douglas K. Brubaker (Co-chair), Dr. Deva D. Chan (Co-chair), Dr. Leopold N. Green, Dr. Yunjie Tong Abstract: Alzheimer's Disease (AD) is a brain disease that compromises cognition. Mouse models have been generated to improve our knowledge of the disease progression and to determine potential treatments. These models, however, are limited in scope and fail to account for the multiple factors that impact AD. It is therefore a challenge to translate therapeutic findings from preclinical testing to clinical trials. To address this translatability gap, I used computational modeling to bridge transcriptomics data from mice and humans and discover potential therapeutics. We performed modeling across species of microglia cells to identify impaired metabolic and inflammatory pathways in human AD, distinguished from those in mice. Based on our findings, I conducted a screening analysis for drugs that expressed opposite signatures to the AD microglia features. In addition, I investigated mouse models comprising different genetic risk factors through different modeling techniques to discover inflammatory mechanisms upregulated in human AD. Through drug screening, I identified insomnia drugs, suggesting a potential role of lack of sleep in AD. I further examined the effects of the insomnia drug, suvorexant, through in vivo cerebrospinal fluid samples. Thus, computational modeling could advance our understanding of the disease and provide a tool to inform us of drug candidates to test for AD.