Gut microbiota have been studied in relation to the pathophysiology of Parkinson'sdisease (PD) due to the early gastrointestinal symptomatology and presence of alpha-synuclein pathology in the enteric nervous system, hypothesized to ascend via the vagal nerve to the central nervous system.
Accordingly, sixteen human case-control studies have published gutmicrobiome composition changes in PD and reported over 100 differentially abundant taxa covering all taxonomic levels from phylum to genus or species, depending on methodology. While certain findings were replicated across several studies, various contradictory findings were reported.
Here, differences in methodologies and the presence of possible confounders in the study populations are assessed for their potential to confound the results of gutmicrobiomestudies in PD. Gutmicrobiomestudies in PD exhibited considerable variability with respect to the study population, sample transport conditions, laboratory protocols and sequencing, bioinformatics pipelines, and biostatistical methods. To move from the current heterogeneous dataset towards clinically relevant biomarkers and the identification of putative therapeutic targets, recommendations are derived from the limitations of the available studies to increase the future comparability of microbiomestudies in PD.
In addition, integration of currently available data on the gutmicrobiome in PD is proposed to identify robust gutmicrobiome profiles in PD. Furthermore, expansion of the current dataset with atypical parkinsonism cohorts, prodromal and treatment-naïve de novo PD subjects, measurements of fecal microbial concentrations and multi-omics assessments are required to provide clinically relevant biomarkers and reveal therapeutic targets within the gutmicrobiome of PD.
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