Differences in the gut microbiome across typical ageing and in Parkinson’s disease Original paper
-
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.
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 is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.
What was studied?
The study investigated the gut microbiome in Parkinson’s disease in the context of normal ageing, asking whether PD-related microbial changes are distinct from, or simply exaggerations of, age-related shifts. Using shotgun metagenomic sequencing with compositional data analysis, the authors compared bacterial diversity, taxonomic profiles, and predicted metabolic pathways across groups. They focused on short-chain fatty acid (SCFA)–producing taxa and butyrate-related functions, given their roles in epithelial integrity, anti-inflammatory signalling, and potential influence on α-synuclein pathology along the microbiota–gut–brain axis. They also modelled associations between microbial features and PD motor/non-motor symptoms, as well as lifestyle factors (dietary fibre, physical activity, sleep efficiency).
Who was studied?
This cross-sectional observational study included 73 community-dwelling adults in Australia: 22 healthy young adults (18–35 years; HY), 33 healthy older adults (50–80 years; HO), and 18 individuals with clinically diagnosed PD aged 50–80 years. Groups were broadly similar in sex and education. By design, HY participants were younger, more physically active, and had lower BMI than older groups. All participants provided stool samples for metagenomic profiling and completed assessments of PD symptomatology (in the PD group), diet (including fibre), physical activity, and sleep (including sleep efficiency), enabling correlation of microbiome data with clinical and behavioural measures.
Most important findings
| Finding | Details |
|---|
| Alpha and beta diversity patterns | Within-sample diversity (alpha diversity) did not differ between Parkinson’s disease (PD) and healthy older (HO) adults, indicating that PD is not simply a “low diversity” state. However, between-sample community structure (beta diversity) differed between PD and HO, pointing to compositional rearrangement rather than global loss of taxa. |
| Reduced Butyricimonas synergistica in PD | A key PD-linked signal was reduced abundance of the butyrate-producing species Butyricimonas synergistica, with lower levels associated with worse non-motor symptoms in PD, supporting a connection between butyrate deficiency, gut barrier dysfunction, and systemic/neuroinflammation. |
| Ageing-related change in Bifidobacterium bifidum | In terms of typical ageing, Bifidobacterium bifidum was more abundant in healthy young (HY) adults compared with healthy older (HO) adults, whereas HO and PD did not differ, suggesting some “PD-like” microbial shifts might actually reflect age-related decline in beneficial taxa. |
| Butyrate pathways vs other metabolic pathways | Predicted butyrate-production pathways were not significantly different among HY, HO, and PD groups, while other metabolic pathways differed among the three groups, hinting at functional redundancy or compensatory changes among butyrate producers. |
| Lifestyle–microbiome associations | Lifestyle–microbiome links emerged: higher sleep efficiency in older adults correlated positively with Roseburia inulinivorans, another short-chain fatty acid (SCFA)–producing species, aligning with emerging evidence for bidirectional sleep–microbiome interactions. Reported associations with fibre intake and physical activity suggest that behaviour and microbiota sit on the same axis as PD risk and progression, though effect sizes in this study appear modest and exploratory. |
Key implications
For clinicians, the message is that PD involves selective shifts in butyrate-producing taxa, not just global microbial loss. The association between lower Butyricimonas synergistica and worse non-motor symptoms positions butyrate-related signatures as candidates for future biomarkers and therapeutic targeting. At the same time, age-related loss of B. bifidum and the sleep–Roseburia link emphasise that any microbiome-based PD intervention must be interpreted against an ageing backdrop and integrated with lifestyle modification (dietary fibre, sleep, activity). Functionally focused microbiome metrics (e.g., SCFA capacity, barrier-supporting taxa) may ultimately be more clinically useful than taxonomic lists alone when designing microbiome-informed strategies for PD management or prevention.
Citation
Nuzum ND, Szymlek-Gay EA, Loke S, Dawson SL, Teo WP, Hendy AM, Loughman A, Macpherson H. Differences in the gut microbiome across typical ageing and in Parkinson’s disease. Neuropharmacology. 2023;235:109566. doi:10.1016/j.neuropharm.2023.109566
Short-chain fatty acids are microbially derived metabolites that regulate epithelial integrity, immune signaling, and microbial ecology. Their production patterns and mechanistic roles provide essential functional markers within microbiome signatures and support the interpretation of MBTIs, MMAs, and systems-level microbial shifts across clinical conditions.