Objective: To investigate whether clinical phenotypes can be predicted by the assessment of gut microbiome and serum inflammatory profile of PD patients.

Background: Recent evidence provides support for involvement of the microbiota-gut-brain axis in Parkinson’s disease (PD) pathogenesis. Earlier have shown that cytokines could play a role in PD pathogenesis. However, differences between clinical PD subgroups regarding these markers still need to be identified.

Method: 112 PD patients in 1,5-3,0 Hoehn-Yahr (mean age 64.4 ± 2.5, 53 males), were evaluated in motor and non-motor domains at the baseline assessment. Clinical subtype (akinetic-rigid (ARS), tremor-dominant (TDS)), disease onset and progression rate were also determined. Study of the fecal samples was performed by real time polymerase chain reaction method and bacteriologically. Cytokines (IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-18, TNF-α, IFN-γ) were measured in serum by ELISA. To identify groups of patients with similar parameters cluster analysis (mclust library) was performed.

Results: In group patients with onset of the diseases before 45 years the level of total bacterial mass and Faecalibacterium prausnitzii was lower than in other patients (p<0,05). Patients who did not receive L-dopa had a lower level of the Escherichia coli, Lactobacillus, Bifidobacterium compared patients compared to patients who received L-dopa (p<0,05). Patients with mild cognitive impairment had a significantly higher level of the Escherichia coli than patients with normal global cognition according to MMSE. Patients with TDS were characterized by a higher level of Bacteroides fragili and IL-10, also a lower level of Lactobacillus compared to ARS (p<0,05). We identified two clusters: cluster 1 had the fastest motor progression, higher level of anxiety and depression, cognitive and autonomic disfunction, higher doses of L-dopa, higher level of the Escherichia coli and Lactobacillus, lower level of IL-1β and IL-4 than cluster 2. 71% in cluster 1 were ARS patients.

Conclusion: Proinflammatory cytokines modulate either directly or through glial cells, enteric nervous system activity which in turn affects to microbiota-gut-brain axis. Gut microbiota may be one of modulator of the pathogenesis of PD and contribute to the interindividual variability of clinical features.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/the-role-of-the-gut-microbial-dysbiosis-and-serum-inflammatory-profile-for-the-discrimination-of-clinical-subtypes-in-parkinsons-disease/