The etiology of Parkinson’s Disease (PD) involves both genetic and environmental factors where inflammation plays a key role. Patients with PD have increased levels of inflammatory cytokines, however it is unclear if inflammation is the cause or result of neurodegeneration. Scientists from the Rush University Medical Center in Chicago recently employed an inflammation-driven model of PD in mice to investigate the utility of lipopolysaccharide-binding protein (LBP) as a biomarker for endotoxin-induced inflammation. Their results showed a significantly reduced amount of LBP in PD patients, indicating an increase of circulating endotoxin due to bacterial translocation. These results establish LBP as a valuable biomarker for identifying PD.