Abstract
IntroductionAlpha-synucleinopathy constituting a characteristic feature of Parkinson’s disease (PD) occurs at all levels of the brain-gut axis including the enteric nervous system (ENS). Lesions in the ENS may be connected with gut inflammation, increased intestinal permeability and dysmotility contributing to the pathogenesis of PD and its gastrointestinal manifestations.AimsTo evaluate fecal calprotectin and zonulin as biomarkers of gut inflammation and intestinal barrier dysfunction in PD patients.MethodsQuantitative evaluation of fecal biomarkers was performed by ELISA tests in 35 PD patients and 20 healthy controls. Additionally, patients filled out a short questionnaire concerning gastrointestinal symptoms.ResultsMedian fecal calprotectin level (μg/g) was significantly higher in PD patients compared to the controls: 54.5 (29.0–137.9) vs. 9.7 (5.2–23.3), p < 0.0001. Applying age-related reference ranges, the increased fecal calprotectin level was found in 43% of PD patients and in none of the control subjects (p < 0.001). No correlation between fecal calprotectin level and PD duration was observed. No statistically significant difference between the groups regarding zonulin level was found. The most frequent bowel symptoms reported by PD patients included constipation (69% of subjects), feeling of incomplete evacuation (51%), bloating (51%), abdominal pain (20%), and alternating bowel movement pattern (17%).ConclusionThe evaluation of fecal calprotectin level may be a useful tool to detect the signs of gut immune system activation present in a remarkable number of PD patients, also in the early stage of the disease. Calprotectin may constitute a critical link between amyloid formation and neuroinflammatory cascades serving as a prospective diagnostic and therapeutic target.
Highlights
Alpha-synucleinopathy constituting a characteristic feature of Parkinson’s disease (PD) occurs at all levels of the brain-gut axis including the enteric nervous system (ENS)
The median fecal calprotectin level was significantly higher in PD patients compared to the controls: 54.5 (29.0– 137.9) vs. 9.7 (5.2–23.3), p < 0.0001 (Figure 1)
Abnormal fecal calprotectin level was found in 43% of all PD patients and in none of the control subjects (p < 0.001)
Summary
Alpha-synucleinopathy constituting a characteristic feature of Parkinson’s disease (PD) occurs at all levels of the brain-gut axis including the enteric nervous system (ENS). Disturbances within the brain-gut-microbiota axis have been increasingly recognized in the pathophysiology of neurodegenerative disorders such as Parkinson’s disease (PD) (Mulak and Bonaz, 2015; Felice et al, 2016). An excessive stimulation of the innate immune system may result in systemic and central nervous system inflammation, while the initiation of alpha-synuclein (α-syn) misfolding may be related to activation of enteric neurons and enteric glial cells (Mulak and Bonaz, 2015; Houser and Tansey, 2017; Stolzenberg et al, 2017). The gut bacteria are able to produce numerous neurotransmitters and neuromodulators such as short-chain fatty acids, their role in neuroinflammation and neurodegeneration has not been yet fully elucidated (Mulak, 2018)
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