Progression of Parkinson's disease is associated with gut dysbiosis: Two-year follow-up study - PubMed (original) (raw)
Progression of Parkinson's disease is associated with gut dysbiosis: Two-year follow-up study
Tomomi Minato et al. PLoS One. 2017.
Expression of concern in
- Expression of Concern: Progression of Parkinson's disease is associated with gut dysbiosis: Two-year follow-up study.
PLOS ONE Editors. PLOS ONE Editors. PLoS One. 2023 Jan 11;18(1):e0280116. doi: 10.1371/journal.pone.0280116. eCollection 2023. PLoS One. 2023. PMID: 36630390 Free PMC article. No abstract available.
Abstract
Background: We previously reported gut dysbiosis in patients with Parkinson's disease (PD).
Objective: The aim of this study is to examine whether gut dysbiosis correlates with the progression of PD.
Methods: We examined changes in gut microbiota and demographic features in 2 years in 36 PD patients.
Results: A change of total UPDRS scores in 2 years was predicted by the counts of Bifidobacterium and Atopobium cluster at year 0 with a correlation coefficient of 0.52. Correlation analysis additionally revealed that low counts of Bifidobacterium and Bacteroides fragilis at year 0 were associated with worsening of UPDRS I scores in 2 years. In addition, low counts of Bifidobacterium at year 0 were associated with worsening of hallucinations/delusions in 2 years. Similarly, low counts of B. fragilis at year 0 were associated with worsening of motivation/initiative in 2 years. The patients were evenly divided into the deteriorated and stable groups based on the degree of worsening of total UPDRS scores. The deteriorated group had lower counts of Bifidobacterium, B. fragilis, and Clostridium leptium than the stable group at year 0 but not at year 2, suggesting that the deteriorated group may demonstrate accelerated lowering of these bacteria at year 0.
Conclusions: The total counts of intestinal bacterial decrease in the course of PD progression. Temporal profiles of lowering of bacterial counts are likely to be different from bacteria to bacteria, and also between the deteriorating and stable groups, which may be able to be exploited to differentiate patients with rapidly and slowly progressive PD pathology.
Conflict of interest statement
Competing Interests: HT and KN are employees of the Yakult Central Institute. This does not alter our adherence to PLOS ONE policies on sharing data and materials. The other authors have no competing interests to declare.
Figures
Fig 1. Prediction of worsening of UPDRS scores using gut microbiota at year 0.
(A) Geometric plot of the counts of Bifidobacterium at year 0 in the deteriorated and stable groups. _P_-value was corrected by the Benjamini and Hochberg method to calculate the false discovery rate (FDR) (_q_-value). (B) A stepwise linear regression analysis for predicting a change of UPDRS scores in 2 years using the counts of 10 bacterial groups/genera/species at year 0 yielded the plotted prediction model, which is comprised of the counts of Bifidobacterium (standardized β = -0.45, p < 0.05) and Atopobium cluster (standardized β = 0.50, p < 0.01). (C, D) Correlation between a change of UPDRS I scores in 2 years and the count of Bifidobacterium at year 0 (C) and the count of B. fragilis group at year 0 (D). (E) Correlation between a change of thought disorder scores (Item 2 in UPDRS I) in 2 years and the count of Bifidobacterium at year 0. (F) Correlation between a change of motivation/initiative scores (Item 4 in UPDRS I) in 2 years and the count of B. fragilis group at year 0. (G, H) Correlation between a change of LBP concentrations in 2 years and the count of L. brevis at year 0 (G) and the count of L. plantarum at year 0 (H). (B, C, D, E, and F) Pearson’s correlation coefficients (r) are indicated with respective _p_-values.
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Grants and funding
The authors acknowledge funding by the Japan Society for the Promotion of Science (JP) (24500458, 15H04840) (http://www.jsps.go.jp/), the Japan Agency for Medical Research and Development (JP) (17gm1010002h0002) (http://www.amed.go.jp/); and Smoking Research Foundation (JP) (http://www.srf.or.jp/). The Yakult Central Institute provided support in the form of salaries for HT and KN, but did not play any further role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. HT and KN blindly quantified intestinal microbiota, and were not involved in the data analysis. HT and KN provided essential experimental information, but did not affect the results and interpretation of our study.
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