Objective: (1) To evaluate the differences in gut microbiota among Parkinson’s disease (PD), atypical parkinsonism (i.e. multiple system atrophy [MSA] and progressive supranuclear palsy [PSP]) and healthy control subjects (HC). (2) To investigate whether specific microbiota taxa may act as modulators of disease progression and clinical phenotype.

Background: Recent evidences support the hypothesis that PD pathology originates into the gut and propagates to the brain by different pathophysiologic pathways. However, findings are heterogeneous probably due to the presence of several confounders.

Methods: We recruited patients with idiopathic PD (n=193, of whom 39 were de novo), PSP (n=22), MSA (n=22), and HC (n=113). Several confounders have been taken into account, including pharmacological therapy and dietary habits. Information on the type of lactation were also recorded. Early-onset PD (≤50 ys) were screened for mutations on parkin, DJ-1, PINK-1 genes.

Results: Despite simple non-parametric comparison of PD patients and HC showed several differences in relative taxa abundances, the number of significant comparisons was greatly reduced after adjusting for multiple confounders. We observed a constant effect of age on almost all abundances. The use of COMT inhibitors appeared to influence the level of several taxa. Overall, PD patients had increased Verrucomicrobia, Christensenellaceae, Lactobacillaceae, and decreased Lachnospiraceae and Ruminococcaceae than HC. Reduced level of Lachnospiraceae was significant in all PD duration strata, while many of these differences were associated with disease progression. De novo PD differed from HC only by lower abundance in Lachnospiraceae. Compared to PD, Lachnospiraceae and Ruminococcaceae were not significantly lower in MSA, while in PSP cases other genera of Ruminococcaceae and Lactobacillaceae were higher and comparable, respectively. Increased Lactobacillaceae, Christensenellaceae, Verrucomicrobia and decreased Lachnospiraceae were associated with worse disease severity, including intellectual impairment and other non-motor symptoms, and axial features (gait disturbances and postural instability).

Conclusions: Gut microbiota may play a role in the pathogenesis of PD and act as modulators of individual differences in disease severity, especially non-dopaminergic features (cognitive functions and axial symptoms).

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MDS Abstracts - https://www.mdsabstracts.org/abstract/unraveling-gut-microbiota-in-parkinsons-disease-and-atypical-parkinsonism/