Parkinson's Disease is a progressive neurodegenerative disorder characterized by motor dysfunction, cognitive and affective symptoms, and emerging evidence of gastrointestinal involvement. Using disease-relevant experimental models, our research investigates how alterations in the gut microbiome and its microbial metabolites may contribute to neuroinflammatory signaling and disease progression. We are particularly interested in determining whether exercise modulates these gut–brain communication pathways, either by reshaping microbial metabolite profiles or altering downstream inflammatory and neuroprotective mechanisms.

Gulf War Illness (GWI) manifests as a constellation of symptoms, notably including gut dysbiosis and neurocognitive impairments. Through our established GWI mouse model, we have identified microbial metabolites as crucial mediators of neuroinflammatory processes, establishing gut dysbiosis as a significant contributor to systemic inflammation that ultimately impacts cognitive function. Our research aims to delineate the precise mechanisms linking these symptomatic domains, and determine how disease-driven alterations in the gut microbiota may modulate neuroinflammatory signaling.

Ceftriaxone is a broad-spectrum beta-lactam antibiotic that significantly depletes gut microbiota, inducing profound shifts in the bacterial composition and structure of the gut microbiome. The resulting loss of commensals essential for intestinal health can trigger systemic inflammatory responses, potentially manifesting as neurocognitive deficits. Given the widespread use of antibiotics in clinical practice, our findings could fundamentally transform prescribing paradigms, facilitating a transition toward more personalized and prophylactic healthcare approaches.

16S rRNA Gene Sequencing

Microbiome Analysis / Bioinformatics

Mouse Models & Behavioral Testing

Immunoblotting 

Immunocytochemistry & Fluorescent Imaging

Mammalian Cell Culture

Proteomic Analysis