Abstract / Summary
Abstract Background and Objectives: Gut inflammation and microbiota dysregulation are increasingly implicated in Parkinson’s disease (PD). Fecal calprotectin, a neutrophil-derived protein and marker of intestinal inflammation, may serve as a non-invasive indicator of gut–brain axis dysfunction in parkinsonian disorders. To evaluate fecal calprotectin levels in idiopathic Parkinson’s disease (IPD) and atypical parkinsonian syndromes—progressive supranuclear palsy (PSP) and multiple system atrophy (MSA)—and examine their relationship with motor and non-motor features. Methods: In this case-control study, 130 patients (IPD = 94, PSP = 23, MSA = 13) and 80 age- and sex-matched healthy controls were enrolled. All participants underwent detailed clinical evaluation, including the movement disorder society–unified Parkinson’s disease rating scale (MDS-UPDRS), Hoehn and Yahr staging, the non-motor symptoms scale (NMSS), the Rome IV criteria for constipation, and the Montreal cognitive assessment (MoCA). Fecal calprotectin (μg/g stool) was quantified using enzyme-linked immunosorbent assay and correlated with clinical parameters. Results: Mean fecal calprotectin was significantly higher in IPD and PSP than in controls ( P < 0.01), whereas MSA showed no significant difference. Elevated fecal calprotectin correlated positively with total NMSS scores ( r ≈ 0.3, P < 0.05) and inversely with MoCA scores, indicating a greater non-motor symptom burden and poorer cognitive performance. No significant correlation was observed with MDS-UPDRS motor scores. Among the NMSS domains, sleep/fatigue, mood/apathy, perceptual problems, memory, and sexual domains exhibited the strongest associations. Conclusions: Fecal calprotectin is elevated in IPD and PSP and is more strongly associated with non-motor than motor manifestations. These findings support intestinal inflammation as a contributor to parkinsonian pathophysiology and highlight fecal calprotectin as a potential biomarker of gut–brain axis dysfunction.