Annals of Indian Academy of Neurology · 2026
Association of Fecal Calprotectin with Motor and Nonmotor Features in Idiopathic Parkinson's Disease and Atypical Parkinsonism.
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Sharma Ashish, Mehta Sahil, Singh Anupam K, Kumar Rajender, Singh Jagdeep, Chakravarty Kamalesh, Lal Vivek
Аннотация
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.
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.