Devon Borg
Of Mice and Meth (Leah’s Subdivision)
UF Center for Cognitive Aging and Memory Fellow
UF MARC Gator STAR (2024-2026)
UF AI Scholars Program (2024 – 2026)
University Scholars Program (2024-2026)
UF Center for Undergraduate Research Travel Award Recipient
McKnight Brain Institute Professional Development Award Recipient
University of Florida Presidential Service Award Recipient
AI Medallion Recipient
I joined the Khoshbouei Lab in 2023 under the mentorship of Leah Phan, where my early research focused on the mechanisms underlying dopaminergic neurodegeneration in Parkinson’s disease. My initial work examined how α-synuclein, a central pathogenic protein in synucleinopathies, differentially impacts dopamine neurons in the substantia nigra pars compacta and ventral tegmental area. Despite their shared neurotransmitter identity, these neuronal populations exhibit striking differences in vulnerability, suggesting that region-specific factors such as metabolic stress, calcium dynamics, and circuit-level demands play a critical role in disease progression. This work contributed to a broader effort to understand the basis of selective neuronal degeneration in Parkinson’s disease.
My current research centers on the neuroimmune response to Candida albicans infection within the central nervous system. This work investigates how acute systemic candidiasis leads to region-specific patterns of fungal infiltration across the brain and how these patterns are shaped by local immune dynamics. In particular, the project examines the role of circulating monocytes in regulating localized neuroimmune defense, as well as how their absence alters fungal burden and immune cell recruitment. Across multiple brain regions, this work highlights pronounced regional heterogeneity in both infection burden and immune response. By framing fungal invasion within a model of region-specific vulnerability and immune regulation, this research expands traditional views of neuropathology to incorporate infection-driven and neuroimmune mechanisms alongside protein aggregation in shaping disease processes.
In parallel, my research has extended into multiple complementary areas that collectively examine dopaminergic dysfunction across different biological contexts. These include studies of transneuronal α-synuclein propagation from the midbrain to the dorsal vagal complex and its downstream consequences, investigations into sex-dependent differences in dopamine dynamics following psychostimulant exposure, and broader questions surrounding circuit-level vulnerability in neurodegenerative disease. Together, these projects reflect a unifying interest in how disruptions at the molecular and cellular level propagate through neural systems to produce complex behavioral and physiological outcomes.
More broadly, my work is guided by a central question: why are certain neuronal populations selectively vulnerable to degeneration, and how do diverse pathological stressors converge on these systems? My research focuses on how these processes disrupt neural circuits and shape disease progression. Through this work, I seek to bridge molecular, circuit-level, and systems neuroscience to better understand the mechanisms driving neurodegeneration and to contribute to the development of targeted, mechanism-based therapies.
