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Background In order to understand how the complex interactions of host with microbiota results in adverse effects on gut and brain, we examine:-
· gastrointestinal microbial predictors of individual, objectively-measured disease facets, recognising (i) that different PD facets may have different drivers (as illustrated with a specific genus of bacterial pathogen, Helicobacter1); (ii) the need to take a trans-kingdom approach.
It is envisaged that incorporating mycobiome and protozome into existing bacteriome data set will be high on agenda.
A systematic review concludes that gastric H. pylori is one pathophysiological driver of Parkinson’s disease (PD), but zoonotic Helicobacter species are also implicated.1 This has led to development of a pan-Helicobacter PCR on saliva, opening the door definition of relevant species.
Currently, emerging picture of our Host Microbiome Interaction: Clinical Pharmacology & Therapeutics Research 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.2
Scope Aim is to pinpoint an individual’s position within an aetiopathogenic model for potential drivers and mediators, predict their trajectory, and recognise opportunities for (and consequences of) disease-modifying intervention. Interventional studies are being planned to allow the move from association to cause effect.
1. Wang, W., et al. Non-Helicobacter pylori Helicobacters, a Treatable Provocateur of Parkinson's Disease: Hypothesis, Evidence and Species Specificity. Int J Mol Sci. 2024 Dec 6;25(23):13123.
2. Augustin A, et al. Faecal metabolite deficit, gut inflammation and diet in Parkinson's disease: Integrative analysis indicates inflammatory response syndrome. Clin Transl Med. 2023 Jan;13(1):e1152.
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