<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Augustin A</submitter><funding>Medical Research Council</funding><funding>National Institute for Health Research (NIHR)</funding><pagination>e1152</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9806009</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Gut-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.&lt;h4>Methods&lt;/h4>We 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.&lt;h4>Results&lt;/h4>Longer colonic transit was linked to deficits in faecal short-chain-fatty acids outside PD, to a 'tryptophan-containing metabolite cluster' overall</pubmed_abstract><journal>Clinical and translational medicine</journal><pubmed_title>Faecal metabolite deficit, gut inflammation and diet in Parkinson's disease: Integrative analysis indicates inflammatory response syndrome.</pubmed_title><pmcid>PMC9806009</pmcid><funding_grant_id>CL-2019-21-002</funding_grant_id><funding_grant_id>MR/S010483/1</funding_grant_id><pubmed_authors>Bjarnason I</pubmed_authors><pubmed_authors>Umamahesan C</pubmed_authors><pubmed_authors>Chekmeneva E</pubmed_authors><pubmed_authors>Ryan S</pubmed_authors><pubmed_authors>Lewis M</pubmed_authors><pubmed_authors>Tucker RM</pubmed_authors><pubmed_authors>Augustin A</pubmed_authors><pubmed_authors>Dobbs RJ</pubmed_authors><pubmed_authors>Ma Y</pubmed_authors><pubmed_authors>Dobbs SM</pubmed_authors><pubmed_authors>Guennec AL</pubmed_authors><pubmed_authors>Kendler-Rhodes A</pubmed_authors><pubmed_authors>Balasubramanian K</pubmed_authors><pubmed_authors>Hayee BH</pubmed_authors><pubmed_authors>DeSouza N</pubmed_authors><pubmed_authors>Ibrahim MAA</pubmed_authors><pubmed_authors>Weller C</pubmed_authors><pubmed_authors>Whelan K</pubmed_authors><pubmed_authors>Taylor D</pubmed_authors><pubmed_authors>Takis P</pubmed_authors><pubmed_authors>Mullish BH</pubmed_authors><pubmed_authors>Charlett A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Faecal metabolite deficit, gut inflammation and diet in Parkinson's disease: Integrative analysis indicates inflammatory response syndrome.</name><description>&lt;h4>Background&lt;/h4>Gut-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.&lt;h4>Methods&lt;/h4>We 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.&lt;h4>Results&lt;/h4>Longer colonic transit was linked to deficits in faecal short-chain-fatty acids outside PD, to a 'tryptophan-containing metabolite cluster' overall</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-05-31T22:56:30.477Z</modification><creation>2024-11-11T18:40:45.136Z</creation></dates><accession>S-EPMC9806009</accession><cross_references><pubmed>36588088</pubmed><doi>10.1002/ctm2.1152</doi></cross_references></HashMap>