Abstract
Objective: An inflammation-driven model of PD has been proposed based on the endotoxin lipopolysaccaride (LPS), a potential source of inflammation in the gastrointestinal system linked to neurotoxicity. Systemic exposure to bacterial endotoxin (LPS) can be determined by measuring plasma LPS binding protein (LBP). We aimed to evaluate whether lipopolysaccharide binding protein (LBP) can be used to distinguish PD subjects from control subjects and to assess whether LBP levels correlate with PD disease severity.Methods: We measured plasma LBP (ng/ml) using an ELISA kit in 94 PD subjects of various stages and 97 control subjects. Disease severity was assessed using the UPDRS and Hoehn and Yahr staging. The LBP level between the PD and control groups was compared using analysis of covariance. Spearman correlation was used to explore the relationship between LBP level and disease severity.Results: The mean LBP level in PD subjects (n = 94) was significantly different from control subjects (n = 95, p = 0.018). In PD subjects, we did not find a correlation between mean LBP level and disease severity.Conclusions: Our data suggests that LBP is one GI biomarker related to LPS induced neurotoxicity. However, there was significant variability in LBP levels within the PD and control groups, limiting its utility as a stand-alone biomarker. This study supports the role of LPS induced neurotoxicity in PD and further exploration of this pathway may be useful in developing sensitive and specific biomarkers for PD.
Highlights
The cause of Parkinson’s disease (PD) is currently unknown
We examined whether reductions in LPS binding protein (LBP) correlate with measures of PD severity
Of the 100 PD subjects enrolled, samples were successfully processed in 94 subjects
Summary
The cause of Parkinson’s disease (PD) is currently unknown. Both environmental and genetic factors have been identified that contribute to PD pathogenesis. The pathology of PD has been found throughout the entire nervous system including the central, peripheral, and enteric nervous system (Braak and Del Tredici, 2008). Environmental factors can trigger an inflammatory cascade in genetically susceptible individuals resulting in neurodegeneration. The intestinal tract and the enteric nervous system may serve as a conduit to the central nervous system. It has been posited that the inflammatory process could gain access to the lower brainstem via the vagal nerve and ascend through the basal mid- and forebrain until it reaches the cerebral cortex, producing various pre-motor and motor symptoms of PD along the way (Braak and Del Tredici, 2008). LPS may be one of the inflammatory triggers involved in this process
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