Objective: To characterize changes in the gut microbiome in de novo PD subjects before and after initiating carbidopa/levodopa

Background: The gastrointestinal microbiome in patients with Parkinson’s disease is rapidly gaining interest in the field. The microbiome may play a role in the development and progression of PD. It may also be a promising biomarker for treatment response. However, the majority of research on the PD microbiome includes patients already taking dopaminergic medication. In order for accurate disease-related biomarkers to be developed, prospective, longitudinal studies on the impact of PD medications on the microbiome are needed. We prospectively assessed the impact of carbidopa/levodopa on the gut microbiome in de novo PD patients initiating this therapy. We also assessed whether phylogenetic diversity predicts treatment response to levodopa.

Method: Subjects with de novo idiopathic PD (n=19) were recruited from the UMass Neurology Clinic. Stool samples were collected before and 90 days after starting carbidopa/levodopa. 16s rRNA gene sequencing was used to identify the organisms present and relative abundances. Kruskal-Wallis test was used to compare the distribution of the phylogenetic diversity of the two groups (alpha and beta diversity pre and post-levodopa), and whether this is associated with change in MDS-UPDRS (categorized as non-responders, modest (<30%), excellent (>30%) responders).

Results: Ninety days after levodopa initiation, subjects had a significant improvement in MDS-UPDRS (mean (SD)=10(12)). There were no significant differences in BMI or dietary habits. Alpha diversity (global diversity) did not differ significantly pre vs post-levodopa. Comparing the non-, modest, and excellent responders, the overall Kruskal-Wallis test showed no significant difference, but the between-group test showed a significant difference in alpha-diversity only between the modest and excellent responder groups.

Conclusion: We preliminarily report that levodopa does not impact the gut microbiome in PD in a short-term, prospective study of de novo subjects. This helps support the existing literature, by suggesting that characteristics of the PD microbiome are likely disease-related rather than medication-related. Larger and longer studies are needed to further validate our findings, and to further explore the role of the microbiome in levodopa response.

References: Keshavarzian, A., Green, S. J., Engen, P. A., Voigt, R. M., Naqib, A., Forsyth, C. B., . . . Shannon, K. M. (2015). Colonic bacterial composition in parkinson’s disease. Movement Disorders : Official Journal of the Movement Disorder Society, 30(10), 1351-1360. doi:10.1002/mds.26307 [doi] Bedarf, J. R., Hildebrand, F., Coelho, L. P., Sunagawa, S., Bahram, M., Goeser, F., . . . Wüllner, U. (2017). Functional implications of microbial and viral gut metagenome changes in early stage L-DOPA-naïve parkinson’s disease patients. Genome Medicine, 9(1), 39. doi:10.1186/s13073-017-0428-y

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MDS Abstracts - https://www.mdsabstracts.org/abstract/effect-of-levodopa-on-gut-microbiome-in-parkinsons-disease-pd/