In summary, our analyses reveal consistent differences in the average gut-microbiota composition between PD patients and controls. The variation among studies is the strongest factor in shaping the data structure, but by accounting for the variability derived by the sampling cohorts we were able to show that the alteration of the gut microbiome in PD is consistent across studies and countries. Additional datasets would help to better quantify the differences observed between PD and controls, helping to identify country-specific effects that we could not resolve. Moreover, the heterogeneity in the available metadata did not allow us to account for more detailed confounding factors such as co-morbidities, drug therapies, and diet. These data would help to further refine the associations between PD and microbiome, and identify taxa that could be mechanistically linked to the disease. The differences in taxa abundances between PD and controls indicate that the gut microbiota of PD patients shares similarities with those of other neurological (e.g., multiple sclerosis) and inflammatory gastrointestinal diseases. Taxa important in maintaining gut integrity and health via the production of SCFA are depleted in PD and this together with the growing evidence of gut and systemic inflammation in PD, points towards an important role of the gut microbiota in modulating the immune function in this disease. Moreover, we were able to identify previously overlooked taxa enriched in PD such as Methanobrevibacter and Butyriciccocaceae, and identified some potentially new metabolic routes through which the microbiota might influence PD. Our findings align with the accumulating evidence indicating gut and systemic inflammation in PD and suggest that the dysbiotic gut microbiota could influence host immune function and be linked to the gastrointestinal symptoms often observed in PD patients.
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