This page is the reference background of the Parkinson's disease page. It works through ten publications — not mixed together, but by two endpoints: separately for the motor and separately for the digestive symptoms. The evidence for the two is radically different, and that is precisely the message of this page.
The connection between Parkinson's disease and the gut flora is one of the most-cited research areas of the past decade. The enthusiasm is understandable — but the clinical evidence is far narrower than that, and anyone who blurs this is not simplifying but misleading.
That there is a real connection between the gut and the brain is supported by several independent observations. In Parkinson's disease alpha-synuclein also accumulates in the bowel wall, and the possibility of spread along the vagus nerve has been described at the level of mechanism.725 In a mouse model the presence of the gut microbiota was necessary for the motor symptoms, the microglial activation and the alpha-synuclein pathology to develop; with an antibiotic the picture eased, and with re-colonisation it returned.198 In humans, the faecal microbiota of people living with Parkinson's disease differs measurably from that of controls, and the difference goes together with the severity of the symptoms.384, 803
Among the clinical endpoints, the improvement of the digestive symptoms is the most consistent signal: in a randomised, placebo-controlled Chinese trial the autonomic and digestive complaints improved meaningfully,802 and the systematic review, too, highlights this.820
The motor benefit is not proven. In the Belgian GUT-PARFECT trial, 12 months after a single nasojejunal treatment the MDS-UPDRS motor score improved by an average of 5.8 points, against 2.7 points for placebo.743 At the same time, in a Finnish, four-centre, colonoscopic randomised trial the primary endpoint did not differ from placebo.744 The overall picture: five randomised trials, 157 patients in total, with results contradicting one another on the motor endpoint — improvement in one, nothing in another, worsening in a third.820
There are no data either that the procedure slows the progression of the disease. The trials have follow-up of a few months or a year, and they measure symptoms, not the course of the disease. No neurological professional guideline recommends FMT in Parkinson's disease.
In the trials the procedure was generally well tolerated, with mild and transient digestive side effects. At one point, however, the picture is not reassuring: in the Finnish trial, in the FMT arm twice as many adverse events occurred as with placebo.744, 820 A particular risk in Parkinson's disease is difficulty swallowing: the preparation is a capsule, and in this patient group aspiration is common and has serious consequences. The minimum requirements of donor screening are discussed separately in the literature;816, 817 our own procedure is described below, in the Safety section.
The animal experiment shows cause and effect, the human studies show association. The two are not the same, and the step between them — whether replacing the gut flora changes the course of the disease in humans — is precisely what is missing. The route of delivery, the dose and the number of donors also differ from trial to trial, which in itself may explain the contradictory results.
Below we ask six questions. For each of them we give the answer first for the motor symptoms, then for the digestive symptoms — in the same breakdown, side by side. This way the difference is visible too, the difference that would be lost in a text that blurred them together.
The MDS-UPDRS III score. This is the standard measure of the movement examination: the examiner scores tremor, rigidity, slowness of movement and gait. It is more objective than a questionnaire, but it is not independent of the examiner's judgement, and the day-to-day fluctuation of Parkinson's disease also plays a part.743, 744
Stool frequency, consistency, an autonomic symptom scale. Simpler and more direct endpoints: the patient records them, and the change can be expressed in days and in stool counts. The non-motor symptom scale (NMSS) complements this.802
Small and divergent. Five randomised trials, 157 patients in total — that is the entire clinical evidence. When an effect is not reproduced in other hands, with another protocol, that in itself is information.820
The same small sample — but pointing one way. The number of patients is no larger here either, but on this endpoint the trials do not contradict one another. This is not strength of evidence but consistency: less of it, but in agreement.
There is no recommendation. Not a single neurological guideline lists FMT among the treatment tools for Parkinson's disease. The research direction is recognised; the clinical application is not.
The treatment of constipation has its own established sequence — fibre, fluids, exercise, osmotic laxative — and this is what the guidelines prescribe. Compared with these, MTT is not first line; it comes into question only if these have been exhausted.
In the protocol and in patient selection. Nasojejunal tube or colonoscopy, single or repeated administration, early or advanced disease — the trials differ in everything. We do not know which difference explains the opposite result.743, 744
In how long it lasts. The follow-up time is short — typically between 12 weeks and 12 months — and we do not know how long the improvement persists, nor whether repeated administration maintains it.820
Dopaminergic therapy. There is no alternative to it, and MTT does not compete with it either. Its place — if it has one — is alongside it for putting bowel function in order, with the agreement of the treating neurologist.
Lifestyle and drug treatment of constipation. These are cheaper, safer and better documented. MTT comes into question when these have been exhausted — and fluid intake and physical activity remain important during the course as well.
| Aspect | Motor symptoms | Digestive symptoms |
|---|---|---|
| What was measured? | MDS-UPDRS III motor score | stool frequency, transit time, autonomic scale |
| What came out? | contradictory: improvement, nothing, worsening | consistent improvement |
| Reliability | 5 RCTs, 157 patients; not reproduced | the same small sample, but pointing one way |
| Guidelines | no recommendation | the established treatment is first line |
| Uncertainty | protocol and patient selection | how long the effect lasts |
| Alternative | dopaminergic therapy — cannot be replaced | fibre, fluids, exercise, osmotic laxative |
| For whom might it come into question? | for this endpoint no one — it cannot be promised | if the established routes have been exhausted, with the neurologist's agreement |
We went through the safety data measured in the publications above: a large pooled review, follow-up over several years, and the caveat that mild, transient complaints are common. What goes into the capsule, however, does not follow from the literature but from our own procedure.
Donor screening. Every donor goes through our DSQ donor screening framework: bacteriological, virological, parasitological and serological testing, stool testing and a detailed questionnaire.
The window period. A recent infection may not yet be detectable at the moment of donation. That is why we keep the donation frozen, in quarantine: for at least eight weeks, and under no circumstances do we release it until the result of the repeat test after the eighth week has arrived. The repeat test covers those infections that could already have occurred before the donation but became detectable only during the eight weeks.
In every case it is under the guidance of your treating physician that the capsules are to be used.
The facts and data on this page come from ten publications in all: four randomised controlled trials, a systematic review, an experimental mouse model, two human observational studies, a mechanism review and two publications dealing with donor screening.
[198] Sampson, T. R., Debelius, J. W., Thron, T. et al. Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkinson's disease Cell 2016. doi:10.1016/j.cell.2016.11.018
In α-synuclein-overexpressing mice modeling Parkinson's disease, gut microbiota were required for motor deficits, microglia activation and α-synuclein pathology. Antibiotic treatment ameliorated, and microbial re-colonization promoted, pathophysiology in adult animals — indicating that postnatal gut-brain signaling modulates disease. Oral administration of specific microbial metabolites to germ-free mice promoted neuroinflammation and motor symptoms. The findings establish a functional link between gut bacteria and synucleinopathies and suggest microbiota-targeting as a therapeutic strategy in PD.Source: references-v2.bib · ref-198
[384] Scheperjans F et al Gut microbiota are related to Parkinson's disease and clinical phenotype Movement Disorders 2015. doi:10.1002/mds.26069
One of the earliest human studies linking the gut flora to Parkinson's disease, comparing stool samples from 72 patients and 72 controls. The Prevotellaceae family was reduced by roughly 78% in patients, and the abundance of Enterobacteriaceae correlated with the severity of postural instability and gait difficulty. The study is cross-sectional: it shows association, not causation — it cannot establish whether the altered flora is a cause or a consequence of the disease.Source: references-v2.bib · ref-384
[725] dos Santos JCC, Oliveira LF, Noleto FM, et al. Gut-microbiome-brain axis: the crosstalk between the vagus nerve, alpha-synuclein and the brain in Parkinson's disease 2023. doi:10.4103/1673-5374.373673
Review article: the gut-microbiome-brain axis in Parkinson's disease — enteric alpha-synuclein aggregation may propagate via the vagus nerve to the CNS, with microbiota metabolites signaling through vagal afferents; a mechanistic synthesis relevant to peripheral intervention targets.Source: references-v2.bib · ref-725
[743] Bruggeman A, Vandendriessche C, Hamerlinck H, De Looze D, Tate DJ, Vuylsteke M, De Commer L, Devolder L, Raes J, Verhasselt B, Laukens D, Vandenbroucke RE, Santens P Safety and efficacy of faecal microbiota transplantation in patients with mild to moderate Parkinson's disease (GUT-PARFECT): a double-blind, placebo-controlled, randomised, phase 2 trial eClinicalMedicine 2024. doi:10.1016/j.eclinm.2024.102563
Double-blind, placebo-controlled, randomised phase 2 trial (Ghent, n=46, aged 50–65, mild to moderate Parkinson's disease): after a single nasojejunal healthy-donor FMT the MDS-UPDRS motor score improved by a mean of 5.8 points at 12 months versus 2.7 points on placebo (autologous stool) (p=0.0235). The difference sits at the edge of clinical relevance and emerged mainly between months 6 and 12. Relief of constipation preceded the motor change. No serious FMT-related adverse events occurred; transient abdominal discomfort did.Source: references-v2.bib · ref-743
[744] Scheperjans F, Levo R, Bosch B, Lääperi M, Pereira PAB, Smolander OP, Aho VTE, Vetkas N, Toivio L, Kainulainen V, Fedorova TD, Lahtinen P, Ortiz R, Kaasinen V, Satokari R, Arkkila P Fecal Microbiota Transplantation for Treatment of Parkinson Disease: A Randomized Clinical Trial JAMA Neurology 2024. doi:10.1001/jamaneurol.2024.2305
NEGATIVE trial. Double-blind, placebo-controlled randomised clinical trial at four Finnish hospitals (48 randomised, 45 in the intention-to-treat analysis; aged 35–75, Hoehn & Yahr 1–3, with documented faecal dysbiosis), single-dose colonic anaerobically prepared FMT versus placebo in a 2:1 ratio. The primary endpoint – change in MDS-UPDRS parts I–III at 6 months – did not differ between groups (0.97 points; 95% CI −5.10 to 7.03; P = .75). Gastrointestinal adverse events were markedly more frequent in the FMT arm (16 [53%] vs 1 [7%]; P = .003). Increases in dopaminergic medication and improvement in several motor and non-motor secondary outcomes were stronger in the placebo group. Microbiota changes were more pronounced after FMT but differed by donor; nevertheless dysbiosis status reversed more often on placebo. Conclusion: FMT was safe but did not offer clinically meaningful improvement.Source: references-v2.bib · ref-744
[802] Cheng, Y., Tan, G., Zhu, Q., et al. Efficacy of fecal microbiota transplantation in patients with Parkinson's disease: clinical trial results from a randomized, placebo-controlled design Gut microbes 2023. doi:10.1080/19490976.2023.2284247
Oral FMT in Parkinson's disease significantly improves autonomic symptoms and microbiota complexity under placebo-controlled conditions; the first Chinese FMT RCT in mild-to-moderate PD patients — safe and clinically promising — 56 mild-to-moderate PD patients (Hoehn-Yahr 1-3), oral FMT vs. placebo. MDS-UPDRS total score group×time effect: B=−6.56 [−12.98; −0.13] (p<0.05). GI symptoms significantly improved in the FMT group. Microbiota complexity markedly increased. No serious adverse events. Oral administration is clinically feasible in PD.Source: references-v2.bib · ref-802
[803] Wallen, Z. D., Demirkan, A., Twa, G., et al. Metagenomics of Parkinson's disease implicates the gut microbiome in multiple disease mechanisms Nat Commun 2022. doi:10.1038/s41467-022-34667-x
This metagenome-wide association study compared 490 Parkinson's disease (PD) patients with 234 controls using deep shotgun fecal sequencing, requiring ANCOM-BC and MaAsLin2 concordance for significance. Over 30% of species, genes and pathways tested were differentially abundant in PD, depicting a widespread dysbiosis. PD-associated species formed polymicrobial clusters that grew or shrank together, with some competing. The PD microbiome was disease-permissive: overabundance of pathogens and immunogenic components, dysregulated neuroactive signaling, preponderance of molecules inducing alpha-synuclein pathology, and overproduction of toxicants, with reduction of anti-inflammatory and neuroprotective factors limiting recovery. The findings support a gut-origin model for PD and identify microbiome targets for intervention.Source: references-v2.bib · ref-803
[816] Kassam, Z., Dubois, N., Ramakrishna, B. et al. Donor Screening for Fecal Microbiota Transplantation N Engl J Med 2019. doi:10.1056/NEJMc1913670
Kassam and colleagues' 2019 New England Journal of Medicine correspondence on 'Donor Screening for Fecal Microbiota Transplantation' was written in the wake of an FDA safety alert reporting two cases of extended-spectrum beta-lactamase (ESBL)-producing E. coli bacteremia — one fatal — transmitted via FMT from a donor not screened for MDROs. The OpenBiome team, the leading US stool bank, summarises updated donor-screening protocols, including ESBL/CRE PCR and culture, and discuss broader implications for biosafety, donor recruitment, and stool-bank operations. The letter directly informed updated FDA, ESCMID and EBP donor-screening recommendations and is the canonical citation for AMR-driven screening intensification.Source: references-v2.bib · ref-816
[817] Rondinella, D., Quaranta, G., Rozera, T., et al. Donor screening for fecal microbiota transplantation with a direct stool testing-based strategy: a prospective cohort study Microbes and infection 2024. doi:10.1016/j.micinf.2024.105341
Direct stool identity testing-based donor screening strategy — Of 277 donations, 99 (36%) were discarded due to pathogen positivity (most common: EPEC n=37, Blastocystis n=20). Among 337 approved aliquots used in FMT: no serious adverse events occurred over 12 weeks.Source: references-v2.bib · ref-817
[820] Nabil, Y. et al. Efficacy and safety of fecal microbiota transplantation in the management of Parkinson's disease: a systematic review BMC Neurology 2025. doi:10.1186/s12883-025-04105-8
Systematic review of faecal microbiota transplantation in Parkinson's disease: five randomised controlled trials, 157 patients in total. Results on the motor endpoint (MDS-UPDRS III) are inconsistent — one trial found significant improvement, another no difference, a third a worsening. Improvement in constipation and other gastrointestinal symptoms is more consistent. The intervention was generally well tolerated, with mild and transient gastrointestinal side effects; in one trial adverse events in the FMT arm were double those on placebo. The authors conclude that FMT may relieve symptoms but that findings are inconsistent, and that larger trials with standardised protocols are needed.Source: references-v2.bib · ref-820
If you want to find out whether your case is suitable, when things happen and what it costs, you will find that on the service page.
The MicroBiome Bank service is not a substitute for professional medical advice, diagnosis or treatment. The decision to use it rests in every case with the treating physician.