Date of Award

Spring 5-10-2025

Level of Access Assigned by Author

Open-Access Thesis

Degree Name

Doctor of Philosophy (PhD)

Department

Biomedical Sciences

First Committee Advisor

Katherine Motyl

Second Committee Member

Calvin Vary

Third Committee Member

Anyonya Guntur

Additional Committee Members

Matthew Lynes

Diana Goode

Abstract

Osteoporosis is a skeletal disease that results from low bone density and strength leading to fracture and ultimately, reduced quality of life and increased mortality. An estimated 1 in 10 adults over the age of 50 in the U.S. have osteoporosis. One of many factors that impact skeletal health includes the use of certain medications that have the unwanted side effect of increased fracture. Referred to as fracture associated drugs (FADs), many FADs are taken to treat nervous system disorders.
/="/"> Utilizing pharmacologic mouse models of atypical antipsychotic (AA) drug, opioid, and selective serotonin reuptake inhibitor (SSRI) treatment, this thesis explores how the nervous system effects bone remodeling evidenced by changes in brown fat activation, micro-RNA expression, and circulating extracellular vesicles related to osteoclast resorption and osteoblast bone formation. Key findings include the propensity for olanzapine, an atypical antipsychotic, to cause trabecular bone loss across different housing temperatures as a modulator of sympathetic and brown fat activation. In contrast, the SSRI sertraline benefits trabecular bone in young wildtype mice, which is distinct from findings from human studies that show SSRI use decreases bone density. Furthermore, this thesis sets a framework to continue to identify novel signaling between nerves and bone via extracellular vesicles using transgenic fluorescent reporter mice. Addressing root causes of bone loss by FADs is important as it may offer new therapeutic targets and prevention strategies and increase overall understanding of signaling between the nervous system and bone.

Available for download on Wednesday, June 10, 2026

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