Evidence map›Paper›PMID 36588088›Full record

ArticleClinical and translational medicine2023

Faecal metabolite deficit, gut inflammation and diet in Parkinson's disease: Integrative analysis indicates inflammatory response syndrome.

Aisha Augustin, Adrien Le Guennec, Chianna Umamahesan, Aidan Kendler-Rhodes, Rosalind M Tucker, Elena Chekmeneva, Panteleimon Takis, Matthew Lewis, Karthik Balasubramanian, Neville DeSouza and 12 more

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
4.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.

  1. Beyond bacteria: a multi-omics view of the gut-brain axis in Parkinson's disease.Frontiers in cellular and infection microbiology · 2026
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  12. Potential ofFrontiers in microbiology · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors at 6 institutions in 3 countries.

Aisha AugustinInstitute of Pharmaceutical Science, King's College London, London, UK.
Adrien Le GuennecNMR Facility, King's College London, London, UK.
Chianna UmamahesanInstitute of Pharmaceutical Science, King's College London, London, UK.
Aidan Kendler-RhodesNutritional Sciences, King's College London, London, UK.
Rosalind M TuckerInstitute of Pharmaceutical Science, King's College London, London, UK.
Elena ChekmenevaNational Phenome Centre, Imperial College London, London, UK.
Panteleimon TakisNational Phenome Centre, Imperial College London, London, UK.
Matthew LewisNational Phenome Centre, Imperial College London, London, UK.
Karthik BalasubramanianInstitute of Pharmaceutical Science, King's College London, London, UK.
Neville DeSouzaThe Maudsley Hospital, London, UK.
Benjamin H MullishDepartment of Metabolism, Digestion and Reproduction, Imperial College, London, UK.ORCID 0000-0001-6300-3100
David TaylorInstitute of Pharmaceutical Science, King's College London, London, UK.
Suzanne RyanImaging, King's College Hospital, London, UK.
Kevin WhelanNutritional Sciences, King's College London, London, UK.
Yun MaInstitute of Liver Studies, King's College Hospital, London, UK.
Mohammad A A IbrahimImmunological Medicine, King's College Hospital, London, UK.
Ingvar BjarnasonGastroenterology, King's College Hospital, London, UK.
Bu' Hussain HayeeGastroenterology, King's College Hospital, London, UK.
André CharlettInstitute of Pharmaceutical Science, King's College London, London, UK.
Sylvia M DobbsInstitute of Pharmaceutical Science, King's College London, London, UK.ORCID 0000-0002-6498-8578
R John DobbsInstitute of Pharmaceutical Science, King's College London, London, UK.
Clive WellerInstitute of Pharmaceutical Science, King's College London, London, UK.
King's College London · GBKing's College Hospital · GBBioanalytica (Switzerland) · CHImperial College London · GBMaudsley Hospital · GBNational Security Agency · US

Funding

Medical Research Council MR/S010483/1
6 · The paper itself

Abstract

backgroundGut-brain axis is widely implicated in the pathophysiology of Parkinson's disease (PD). We take an integrated approach to considering the gut as a target for disease-modifying intervention, using continuous measurements of disease facets irrespective of diagnostic divide.

methodsWe characterised 77 participants with diagnosed-PD, 113 without, by dietary/exogenous substance intake, faecal metabolome, intestinal inflammation, serum cytokines/chemokines, clinical phenotype including colonic transit time. Complete-linkage hierarchical cluster analysis of metabolites discriminant for PD-status was performed.

resultsLonger colonic transit was linked to deficits in faecal short-chain-fatty acids outside PD, to a 'tryptophan-containing metabolite cluster' overall. Phenotypic cluster analysis aggregated colonic transit with brady/hypokinesia, tremor, sleep disorder and dysosmia, each individually associated with tryptophan-cluster deficit. Overall, a faster pulse was associated with deficits in a metabolite cluster including benzoic acid and an imidazole-ring compound (anti-fungals) and vitamin B3 (anti-inflammatory) and with higher serum CCL20 (chemotactic for lymphocytes/dendritic cells towards mucosal epithelium). The faster pulse in PD was irrespective of postural hypotension. The benzoic acid-cluster deficit was linked to (well-recognised) lower caffeine and alcohol intakes, tryptophan-cluster deficit to higher maltose intake. Free-sugar intake was increased in PD, maltose intake being 63% higher (p = .001). Faecal calprotectin was 44% (95% CI 5%, 98%) greater in PD [p = .001, adjusted for proton-pump inhibitors (p = .001)], with 16% of PD-probands exceeding a cut-point for clinically significant inflammation compatible with inflammatory bowel disease. Higher maltose intake was associated with exceeding this calprotectin cut-point.

conclusionsEmerging picture is of (i) clinical phenotype being described by deficits in microbial metabolites essential to gut health; (ii) intestinal inflammation; (iii) a systemic inflammatory response syndrome.

Indexed as

Parkinson DiseaseBenzoatesDietHumansInflammationLeukocyte L1 Antigen ComplexMaltoseTryptophanBenzoatesLeukocyte L1 Antigen ComplexMaltoseTryptophanfaecal metabolomeintestinal inflammationParkinson's diseasesystemic immunome

Identifiers

PMID36588088
PMCPMC9806009
OpenAlexW4313453362

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.