Oral and gut microbiome profiles in people with early idiopathic Parkinson’s disease Original paper
Researched by:
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Dr. Umar
ID
Dr. Umar
Read MoreClinical Pharmacist and Clinical Pharmacy Master’s candidate focused on antibiotic stewardship, AI-driven pharmacy practice, and research that strengthens safe and effective medication use. Experience spans digital health research with Bloomsbury Health (London), pharmacovigilance in patient support programs, and behavioral approaches to mental health care. Published work includes studies on antibiotic use and awareness, AI applications in medicine, postpartum depression management, and patient safety reporting. Developer of an AI-based clinical decision support system designed to enhance antimicrobial stewardship and optimize therapeutic outcomes.
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Dr. Umar
Read More
Researched by:
-
Dr. Umar
ID
Dr. Umar
Read More
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Karen Pendergrass
Location
United States of America
Sample Site
Feces
Saliva
Species
Homo sapiens
What was studied?
Oral and gut microbiome signatures in early Parkinson’s disease were examined using shallow shotgun metagenomics of paired saliva and stool from a large matched case–control cohort. The authors tested whether specific taxonomic, functional, and network features in saliva and stool constitute reproducible PD microbiome signatures, how these patterns relate to constipation and orthostatic hypotension, and whether oral or gut profiles better classify PD status.
Who was studied?
Investigators recruited 774 participants from the 23andMe research program, aged 50–69 years, all of European genetic ancestry and living in the United States; after quality control, analyses included 445 PD cases and 221 controls for stool, and 438 cases and 220 controls for saliva. PD participants had self-reported early idiopathic PD (<5–8 years duration), while controls had neither PD nor a first-degree relative with PD. Exclusion criteria for both groups were recent antibiotics, vegetarian/vegan diet, high-penetrance LRRK2 G2019S or GBA N370S variants, and non-US residence.
Most important findings
In early Parkinson’s disease, oral and gut microbiome signatures in early Parkinson’s disease show higher stool richness, especially in those with constipation and greater autonomic symptom burden, while saliva changes are driven more by compositional shifts than by diversity. Both saliva and stool clearly separate PD from controls based on beta-diversity, and microbial networks are fragmented despite increased richness.
| Feature / Taxa | PD-associated pattern |
|---|---|
| Stool alpha-diversity (richness) | Increased in PD vs controls; strongest in constipated PD and scales with autonomic symptom burden. |
| Beta-diversity (stool & saliva) | Sørensen distances clearly separate PD from controls, driven by presence/absence of (often rare) taxa. |
| Autonomic symptoms | In PD, higher stool richness tracks with constipation and orthostatic hypotension; not seen in controls. |
| Saliva community | Composition (not richness) shifts with autonomic scores and flossing frequency in PD. |
| Microbial networks (stool & saliva) | Fewer co-abundance links and fragmented KEGG functional networks in PD, implying a less integrated ecosystem. |
| Enriched taxa | Streptococcus mutans, Bifidobacterium dentium, Streptococcus vestibularis, other oral-type streptococci. |
| Depleted taxa | Prevotella loescheii, multiple Neisseria spp., Parabacteroides distasonis, Ruminococcus gnavus. |
| Classifier performance (saliva OTUs) | Saliva OTU profiles AUC ≈ 0.76; with survey data AUC ≈ 0.78 for PD vs controls classification. |
Early PD is marked by increased stool richness, fragmented microbial networks, and a distinct oral–gut taxonomic signature, with saliva subspecies profiles providing the strongest diagnostic signal.
Key implications
For clinicians, these data support oral and gut microbiome signatures in early Parkinson’s disease as integrated markers of disease burden rather than isolated gut phenomena. Increased gut richness, plus disrupted co-abundance networks and enrichment of oral pathobionts, suggest weakened host control and a shift toward pro-inflammatory, carbohydrate-adapted communities across the gastrointestinal tract. Saliva, sampled non-invasively, provided the strongest microbiome signal for case–control discrimination, positioning subspecies-level salivary taxa—such as S. mutans, S. vestibularis, B. dentium enrichment, and Neisseria/Prevotella depletion—as high-priority candidates for microbiome signature databases and future biomarker panels. Because the study is cross-sectional, the microbiome patterns cannot yet be considered causal, but they delineate practical microbial targets for longitudinal risk stratification, trials modulating oral–gut communities, and mechanistic work along the microbiota–gut–brain axis.
Citation
Stagaman K, Kmiecik MJ, Wetzel M, Aslibekyan S, Filshtein Sonmez T, Fontanillas P, 23andMe Research Team, Tung J, Holmes MV, Walk ST, Houser MC, Norcliffe-Kaufmann L. Oral and gut microbiome profiles in people with early idiopathic Parkinson’s disease. Communications Medicine. 2024;4:209. doi:10.1038/s43856-024-00630-8