Think of the gut microbiome as a bustling city, a metropolis teeming with microbes and their functions. Just like any city, the microbiome has its own delicate balance that can be disrupted. In Parkinson’s disease (PD), this disruption is evident, with certain beneficial bacteria being underrepresented. But how does this change over time? And what about the effects of device-assisted therapies (DAT)? Researchers conducted a longitudinal study to find out! They tracked the gut microbiome profiles of PD patients on standard therapies and those starting DAT. Interestingly, they found that specific bacteria were consistently altered in PD patients compared to healthy controls. However, the initiation of DAT did not have a sustained effect on the gut microbiome. Plus, combining microbiota data with nutritional profiles improved predictions of disease progression. This study provides valuable insights into the complex relationship between the gut microbiome and PD, paving the way for potential future interventions. Want to learn more about how our tiny microbial citizens may impact Parkinson’s? Check out the full research article!

BackgroundAltered gut microbiome (GM) composition has been established in Parkinson’s disease (PD). However, few studies have longitudinally investigated the GM in PD, or the impact of device-assisted therapies.ObjectivesTo investigate the temporal stability of GM profiles from PD patients on standard therapies and those initiating device-assisted therapies (DAT) and define multivariate models of disease and progression.MethodsWe evaluated validated clinical questionnaires and stool samples from 74 PD patients and 74 household controls (HCs) at 0, 6, and 12 months. Faster or slower disease progression was defined from levodopa equivalence dose and motor severity measures. 19 PD patients initiating Deep Brain Stimulation or Levodopa-Carbidopa Intestinal Gel were separately evaluated at 0, 6, and 12 months post-therapy initiation.ResultsPersistent underrepresentation of short-chain fatty-acid-producing bacteria, Butyricicoccus, Fusicatenibacter, Lachnospiraceae ND3007 group, and Erysipelotrichaceae UCG-003, were apparent in PD patients relative to controls. A sustained effect of DAT initiation on GM associations with PD was not observed. PD progression analysis indicated that the genus Barnesiella was underrepresented in faster progressing PD patients at t = 0 and t = 12 months. Two-stage predictive modeling, integrating microbiota abundances and nutritional profiles, improved predictive capacity (change in Area Under the Curve from 0.58 to 0.64) when assessed at Amplicon Sequence Variant taxonomic resolution.ConclusionWe present longitudinal GM studies in PD patients, showing persistently altered GM profiles suggestive of a reduced butyrogenic production potential. DATs exerted variable GM influences across the short and longer-term. We found that specific GM profiles combined with dietary factors improved prediction of disease progression in PD patients.

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