Abstract
Gut microbiome composition is altered in Parkinson’s disease (PD), the fastest-growing neurological condition, that is characterized by neurodegeneration, motor dysfunction, and is frequently accompanied by gastrointestinal (GI) symptoms. Notably, microbial taxa with anti-inflammatory properties are consistently depleted in PD patients compared to controls. To explore whether specific gut bacteria may be disease-protective, we assembled a microbial consortium of 8 human-associated taxa that are reduced in individuals with PD. Treatment of α-synuclein overexpressing (Thy1-ASO) mice, an animal model of PD, with this consortium improved motor and GI deficits. A single bacterial species from this consortium, Faecalibacterium prausnitzii, was sufficient to correct gut microbiome deviations in Thy1-ASO mice, induce anti-inflammatory immune responses, and promote protective colonic gene expression profiles. Accordingly, oral treatment with F. prausnitzii robustly ameliorated motor and GI deficits and reduced α-synuclein aggregates in the brain. These findings support the emerging hypothesis of functional contributions by the microbiome to PD outcomes, and embolden the development of potential probiotic therapies to treat motor and non-motor symptoms.
Similar content being viewed by others
Data availability
The data, code, protocols, and key lab materials used and generated in this study are listed in the Key Resource Table (Supplementary Table 2, also available at https://doi.org/10.5281/zenodo.17137678) alongside their persistent identifiers. For microbiome analysis data, raw FASTQ files were deposited in the SRA (PRJNA1259538) along with sample metadata, and code to generate data, figures, and statistics is available at https://doi.org/10.5281/zenodo.17128213. For RNA sequencing analysis data, raw FASTQ files were deposited in the SRA (PRJNA1308739) along with sample metadata, and code to generate data, figures, and statistics is available at https://doi.org/10.5281/zenodo.17981510. Raw flow cytometry data were deposited to Zenodo (https://doi.org/10.5281/zenodo.16929959) along with sample metadata. All other raw data and analyses, including behavior data analysis, original blot images, multiplex, and VFA data, can be found at https://doi.org/10.5281/zenodo.17137678.
References
Tysnes, O.-B. & Storstein, A. Epidemiology of Parkinson’s disease. J. Neural Transm. (Vienna) 124, 901–905 (2017).
Poewe, W. et al. Parkinson disease. Nat. Rev. Dis. Prim. 3, 17013 (2017).
Dorsey, E. R., Sherer, T., Okun, M. S. & Bloem, B. R. The emerging evidence of the Parkinson pandemic. J. Parkinsons Dis. 8, S3–S8 (2018).
Koga, S., Sekiya, H., Kondru, N., Ross, O. A. & Dickson, D. W. Neuropathology and molecular diagnosis of synucleinopathies. Mol. Neurodegener. 16, 83 (2021).
Hawkes, C. H., Del Tredici, K. & Braak, H. A timeline for Parkinson’s disease. Parkinsonism Relat. Disord. 16, 79–84 (2010).
Pardo-Moreno, T. et al. Current treatments and new, tentative therapies for Parkinson’s disease. Pharmaceutics 15, 770 (2023).
Parkinson, J. An essay on the shaking palsy. JNP 14, 223–236 (2002).
Forsyth, C. B. et al. Increased intestinal permeability correlates with sigmoid mucosa alpha-synuclein staining and endotoxin exposure markers in early Parkinson’s disease. PLoS ONE 6, e28032 (2011).
Yang, D. et al. The role of the gut microbiota in the pathogenesis of Parkinson’s disease. Front. Neurol. 10, 1155 (2019).
Pellicano, C. et al. Prodromal non-motor symptoms of Parkinson’s disease. Neuropsychiatr. Dis. Treat. 3, 145–151 (2007).
Galbiati, A., Verga, L., Giora, E., Zucconi, M. & Ferini-Strambi, L. The risk of neurodegeneration in REM sleep behavior disorder: a systematic review and meta-analysis of longitudinal studies. Sleep. Med. Rev. 43, 37–46 (2019).
Postuma, R. B. & Berg, D. Advances in markers of prodromal Parkinson disease. Nat. Rev. Neurol. 12, 622–634 (2016).
Dorsey, E. R., De Miranda, B. R., Horsager, J. & Borghammer, P. The body, the brain, the environment, and Parkinson’s disease. J. Parkinsons Dis. 14, 363–381 (2024).
Berg, D. et al. Prodromal Parkinson disease subtypes - key to understanding heterogeneity. Nat. Rev. Neurol. 17, 349–361 (2021).
Braak, H., Rüb, U., Gai, W. P. & Del Tredici, K. Idiopathic Parkinson’s disease: possible routes by which vulnerable neuronal types may be subject to neuroinvasion by an unknown pathogen. J. Neural Transm. (Vienna) 110, 517–536 (2003).
Kim, S. et al. Transneuronal propagation of pathologic α-synuclein from the gut to the brain models Parkinson’s disease. Neuron 103, 627–641.e7 (2019).
Challis, C. et al. Gut-seeded α-synuclein fibrils promote gut dysfunction and brain pathology specifically in aged mice. Nat. Neurosci. 23, 327–336 (2020).
Liu, B. et al. Vagotomy and Parkinson disease: a Swedish register-based matched-cohort study. Neurology 88, 1996–2002 (2017).
Svensson, E. et al. Vagotomy and subsequent risk of Parkinson’s disease. Ann. Neurol. 78, 522–529 (2015).
Sampson, T. The impact of indigenous microbes on Parkinson’s disease. Neurobiol. Dis. 135, 104426 (2020).
Hill-Burns, E. M. et al. Parkinson’s disease and Parkinson’s disease medications have distinct signatures of the gut microbiome. Mov. Disord. 32, 739–749 (2017).
Aho, V. T. E. et al. Gut microbiota in Parkinson’s disease: Temporal stability and relations to disease progression. EBioMedicine 44, 691–707 (2019).
Bedarf, J. R. et al. Functional implications of microbial and viral gut metagenome changes in early stage L-DOPA-naïve Parkinson’s disease patients. Genome Med. 9, 39–39 (2017).
Wallen, Z. D. et al. Metagenomics of Parkinson’s disease implicates the gut microbiome in multiple disease mechanisms. Nat. Commun. 13, 6958 (2022).
Elford, J. D., Becht, N., Garssen, J., Kraneveld, A. D. & Perez-Pardo, P. Buty and the beast: the complex role of butyrate in Parkinson’s disease. Front. Pharm. 15, 1388401 (2024).
Dalile, B., Van Oudenhove, L., Vervliet, B. & Verbeke, K. The role of short-chain fatty acids in microbiota–gut–brain communication. Nat. Rev. Gastroenterol. Hepatol. 16, 461–478 (2019).
Fernández, J. et al. Colon microbiota fermentation of dietary prebiotics towards short-chain fatty acids and their roles as anti-inflammatory and antitumour agents: a review. J. Funct. Foods 25, 511–522 (2016).
Hamilton, A. M., Krout, I. N., White, A. C. & Sampson, T. R. Microbiome-based therapeutics for Parkinson’s disease. Neurotherapeutics 21, e00462 (2024).
Tan, A. H. et al. Probiotics for Constipation in Parkinson disease: a randomized placebo-controlled study. Neurology 96, e772–e782 (2021).
Ibrahim, A. et al. Multi-strain probiotics (Hexbio) containing MCP BCMC strains improved constipation and gut motility in Parkinson’s disease: a randomised controlled trial. PLoS ONE 15, e0244680 (2020).
Barichella, M. et al. Probiotics and prebiotic fiber for constipation associated with Parkinson disease: an RCT. Neurology 87, 1274–1280 (2016).
Keshavarzian, A. et al. Colonic bacterial composition in Parkinson’s disease. Mov. Disord. 30, 1351–1360 (2015).
Unger, M. M. et al. Short chain fatty acids and gut microbiota differ between patients with Parkinson’s disease and age-matched controls. Parkinsonism Relat. Disord. 32, 66–72 (2016).
Li, W. et al. Structural changes of gut microbiota in Parkinson’s disease and its correlation with clinical features. Sci. China Life Sci. 60, 1223–1233 (2017).
Petrov, V. A. et al. Analysis of gut microbiota in patients with Parkinson’s disease. Bull. Exp. Biol. Med. 162, 734–737 (2017).
Boktor, J. C. et al. Integrated multi-cohort analysis of the Parkinson’s disease gut metagenome. Mov. Disord. 38, 399–409 (2023).
Sokol, H. et al. Faecalibacterium prausnitzii is an anti-inflammatory commensal bacterium identified by gut microbiota analysis of Crohn disease patients. Proc. Natl. Acad. Sci. USA 105, 16731–16736 (2008).
Quévrain, E. et al. Identification of an anti-inflammatory protein from Faecalibacterium prausnitzii, a commensal bacterium deficient in Crohn’s disease. Gut 65, 415–425 (2016).
Martín, R., Bermúdez-Humarán, L. G. & Langella, P. Searching for the bacterial effector: the example of the multi-skilled commensal bacterium Faecalibacterium prausnitzii. Front Microbiol 9, 346 (2018).
Zhou, L. et al. Faecalibacterium prausnitzii produces butyrate to maintain Th17/Treg balance and to ameliorate colorectal colitis by inhibiting histone deacetylase 1. Inflamm. Bowel Dis. 24, 1926–1940 (2018).
Li, H.-X. et al. Inflammatory bowel disease and risk of Parkinson’s disease: evidence from a meta-analysis of 14 studies involving more than 13.4 million individuals. Front. Med. (Lausanne) 10, 1137366 (2023).
Zhu, Y. et al. Association between inflammatory bowel diseases and Parkinson’s disease: systematic review and meta-analysis. Neural Regen. Res. 17, 344–353 (2022).
Chesselet, M.-F. et al. A progressive mouse model of Parkinson’s disease: the Thy1-aSyn (“Line 61”) mice. Neurotherapeutics 9, 297–314 (2012).
Richter, F., Stanojlovic, M., Käufer, C., Gericke, B. & Feja, M. A mouse model to test novel therapeutics for Parkinson’s disease: an update on the Thy1-aSyn (‘line 61’) mice. Neurotherapeutics 20, 97–116 (2023).
Anderson, J. P. et al. Phosphorylation of Ser-129 is the dominant pathological modification of alpha-synuclein in familial and sporadic Lewy body disease. J. Biol. Chem. 281, 29739–29752 (2006).
Geistlinger, L. et al. BugSigDB captures patterns of differential abundance across a broad range of host-associated microbial signatures. Nat. Biotechnol. 42, 790–802 (2024).
Martín, R. et al. Faecalibacterium: a bacterial genus with promising human health applications. FEMS Microbiol. Rev. 47, fuad039 (2023).
Yang, X., Qian, Y., Xu, S., Song, Y. & Xiao, Q. Longitudinal analysis of fecal microbiome and pathologic processes in a rotenone induced mice model of Parkinson’s disease. Front. Aging Neurosci. 9, 441 (2017).
Sampson, T. R. et al. Alpha synuclein overexpression can drive microbiome dysbiosis in mice. Sci. Rep. 15, 4014 (2025).
Abdel-Haq, R. et al. A prebiotic diet modulates microglial states and motor deficits in α-synuclein overexpressing mice. eLife 11, e81453 (2022).
Aktas, B. Gut Microbial alteration in MPTP mouse model of Parkinson disease is administration regimen dependent. Cell. Mol. Neurobiol. 43, 2815–2829 (2023).
Yan, Y. et al. Gut microbiota and metabolites of α-synuclein transgenic monkey models with early stage of Parkinson’s disease. NPJ Biofilms Microbiomes 7, 69 (2021).
Wrzosek, L. et al. Bacteroides thetaiotaomicron and Faecalibacterium prausnitzii influence the production of mucus glycans and the development of goblet cells in the colonic epithelium of a gnotobiotic model rodent. BMC Biol. 11, 61 (2013).
Miquel, S. et al. Identification of metabolic signatures linked to anti-inflammatory effects of Faecalibacterium prausnitzii. mBio 6, e00300-15 (2015).
Kim, H., Jeong, Y., Kang, S., You, H. J. & Ji, G. E. Co-Culture with Bifidobacterium catenulatum improves the growth, gut colonization, and butyrate production of Faecalibacterium prausnitzii: in vitro and in vivo studies. Microorganisms 8, 788 (2020).
Moon, J. et al. Faecalibacterium prausnitzii alleviates inflammatory arthritis and regulates IL-17 production, short chain fatty acids, and the intestinal microbial flora in experimental mouse model for rheumatoid arthritis. Arthritis Res. Ther. 25, 130 (2023).
Bredon, M. et al. Faecalibaterium prausnitzii strain EXL01 boosts efficacy of immune checkpoint inhibitors. Oncoimmunology 13, 2374954 (2024).
Shi, Z. et al. Faecalibacterium prausnitzii promotes anti-PD-L1 efficacy in natural killer/T-cell lymphoma by enhancing antitumor immunity. BMC Med. 23, 387 (2025).
Park, S.-Y. et al. Alpha-synuclein-specific regulatory T cells ameliorate Parkinson’s disease progression in mice. Int. J. Mol. Sci. 24, 15237 (2023).
Reynolds, A. D., Banerjee, R., Liu, J., Gendelman, H. E. & Mosley, R. L. Neuroprotective activities of CD4+CD25+ regulatory T cells in an animal model of Parkinson’s disease. J. Leukoc. Biol. 82, 1083–1094 (2007).
Arce-Sillas, A. et al. Increased levels of regulatory T cells and IL-10-producing regulatory B cells are linked to improved clinical outcome in Parkinson’s disease: a 1-year observational study. J. Neural Transm. (Vienna) 131, 901–916 (2024).
Miquel, S. et al. Ecology and metabolism of the beneficial intestinal commensal bacterium Faecalibacterium prausnitzii. Gut Microbes 5, 146–151 (2014).
Lenoir, M. et al. Butyrate mediates anti-inflammatory effects of Faecalibacterium prausnitzii in intestinal epithelial cells through Dact3. Gut Microbes 12, 1–16 (2020).
Mohebali, N. et al. Faecalibacterium prausnitzii, Bacteroides faecis and Roseburia intestinalis attenuate clinical symptoms of experimental colitis by regulating Treg/Th17 cell balance and intestinal barrier integrity. Biomed. Pharmacother. 167, 115568 (2023).
Jabara, H. H. et al. A missense mutation in TFRC, encoding transferrin receptor 1, causes combined immunodeficiency. Nat. Genet. 48, 74–78 (2016).
Bolen, M. L. et al. Peripheral blood immune cells from individuals with Parkinson’s disease or inflammatory bowel disease share deficits in iron storage and transport that are modulated by non-steroidal anti-inflammatory drugs. Neurobiol. Dis. 207, 106794 (2025).
Sabbir, M. G. Loss of calcium/calmodulin-dependent protein kinase kinase 2, transferrin, and transferrin receptor proteins in the temporal cortex of Alzheimer’s patients postmortem is associated with abnormal iron homeostasis: implications for patient survival. Front. Cell Dev. Biol. 12, 1469751 (2024).
Ayton, S., Lei, P., Mclean, C., Bush, A. I. & Finkelstein, D. I. Transferrin protects against Parkinsonian neurotoxicity and is deficient in Parkinson’s substantia nigra. Signal Transduct. Target Ther. 1, 16015 (2016).
Rentzos, M. et al. Circulating interleukin-15 and RANTES chemokine in Parkinson’s disease. Acta Neurol. Scand. 116, 374–379 (2007).
Tang, P. et al. Correlation between serum RANTES levels and the severity of Parkinson’s disease. Oxid. Med. Cell. Longev. 2014, 208408 (2014).
Galiano-Landeira, J., Torra, A., Vila, M. & Bové, J. CD8 T cell nigral infiltration precedes synucleinopathy in early stages of Parkinson’s disease. Brain 143, 3717–3733 (2020).
Williams, G. P. et al. CD4 T cells mediate brain inflammation and neurodegeneration in a mouse model of Parkinson’s disease. Brain 144, 2047–2059 (2021).
Sekijima, Y. Recent progress in the understanding and treatment of transthyretin amyloidosis. J. Clin. Pharm. Ther. 39, 225–233 (2014).
Maetzler, W. et al. Serum and cerebrospinal fluid levels of transthyretin in Lewy body disorders with and without dementia. PLoS ONE 7, e48042 (2012).
Sárkány, Z. et al. Transthyretin has conformation-selective proteolytic activity against α-synuclein. Preprint at bioRxiv https://doi.org/10.1101/2023.08.10.552896 (2023).
Cardoso, B. R., Roberts, B. R., Bush, A. I. & Hare, D. J. Selenium, selenoproteins and neurodegenerative diseases. Metallomics 7, 1213–1228 (2015).
Xu, K. et al. Engineered selenium/human serum albumin nanoparticles for efficient targeted treatment of Parkinson’s disease via oral gavage. ACS Nano 17, 19961–19980 (2023).
De Miranda, B. R., Goldman, S. M., Miller, G. W., Greenamyre, J. T. & Dorsey, E. R. Preventing Parkinson’s disease: an environmental agenda. J. Parkinsons Dis. 12, 45–68 (2022).
Scheperjans, F. et al. Gut microbiota are related to Parkinson’s disease and clinical phenotype. Mov. Disord. 30, 350–358 (2015).
Tan, A. H. et al. Small intestinal bacterial overgrowth in Parkinson’s disease. Parkinsonism Relat. Disord. 20, 535–540 (2014).
Sampson, T. R. et al. Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkinson’s disease. Cell 167, 1469–1480.e12 (2016).
Choi, J. G. et al. Oral administration of Proteus mirabilis damages dopaminergic neurons and motor functions in mice. Sci. Rep. 8, 1275 (2018).
Matheoud, D. et al. Intestinal infection triggers Parkinson’s disease-like symptoms in Pink1−/− mice. Nature 571, 565–569 (2019).
Zhao, Z. et al. Fecal microbiota transplantation protects rotenone-induced Parkinson’s disease mice via suppressing inflammation mediated by the lipopolysaccharide-TLR4 signaling pathway through the microbiota–gut–brain axis. Microbiome 9, 226–226 (2021).
Sun, M.-F. et al. Neuroprotective effects of fecal microbiota transplantation on MPTP-induced Parkinson’s disease mice: gut microbiota, glial reaction and TLR4/TNF-α signaling pathway. Brain Behav. Immun. 70, 48–60 (2018).
Zhong, Z. et al. Fecal microbiota transplantation exerts a protective role in MPTP-induced Parkinson’s disease via the TLR4/PI3K/AKT/NF-κB pathway stimulated by α-synuclein. Neurochem. Res. 46, 3050–3058 (2021).
Xie, Z. et al. Healthy human fecal microbiota transplantation into mice attenuates MPTP-induced neurotoxicity via AMPK/SOD2 pathway. Aging Dis. 14, 2193–2214 (2023).
Bruggeman, A. et al. 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 71, 102563 (2024).
Cheng, Y. et al. Efficacy of fecal microbiota transplantation in patients with Parkinson’s disease: clinical trial results from a randomized, placebo-controlled design. Gut Microbes 15, 2284247 (2023).
DuPont, H. L. et al. Fecal microbiota transplantation in Parkinson’s disease—a randomized repeat-dose, placebo-controlled clinical pilot study. Front. Neurol. 14, 1104759 (2023).
Scheperjans, F. et al. Fecal microbiota transplantation for treatment of Parkinson disease: a randomized clinical trial. JAMA Neurol. e242305 (2024) https://doi.org/10.1001/jamaneurol.2024.2305.
Peter, I. et al. Anti-tumor necrosis factor therapy and incidence of Parkinson disease among patients with inflammatory bowel disease. JAMA Neurol. 75, 939–946 (2018).
Gao, X., Chen, H., Schwarzschild, M. A. & Ascherio, A. Use of ibuprofen and risk of Parkinson disease. Neurology 76, 863–869 (2011).
Barnum, C. J. et al. Peripheral administration of the selective inhibitor of soluble tumor necrosis factor (TNF) XPro®1595 attenuates nigral cell loss and glial activation in 6-OHDA hemiparkinsonian rats. J. Parkinsons Dis. 4, 349–360 (2014).
Swiątkiewicz, M., Zaremba, M., Joniec, I., Członkowski, A. & Kurkowska-Jastrzębska, I. Potential neuroprotective effect of ibuprofen, insights from the mice model of Parkinson’s disease. Pharm. Rep. 65, 1227–1236 (2013).
Zhao, P. et al. Neuroprotective effects of fingolimod in mouse models of Parkinson’s disease. FASEB J. 31, 172–179 (2017).
Nie, K. et al. Roseburia intestinalis: a beneficial gut organism from the discoveries in genus and species. Front. Cell. Infect. Microbiol. 11, 757718 (2021).
Zhu, C. et al. Roseburia intestinalis inhibits interleukin‑17 excretion and promotes regulatory T cells differentiation in colitis. Mol. Med. Rep. 17, 7567–7574 (2018).
Han, H. S. et al. Roseburia intestinalis-derived extracellular vesicles ameliorate colitis by modulating intestinal barrier, microbiome, and inflammatory responses. J. Extracell. Vesicles 13, e12487 (2024).
Choi, S. I. et al. The protective effect of Roseburia faecis against repeated water avoidance stress-induced irritable bowel syndrome in a Wister rat model. J. Cancer Prev. 28, 93–105 (2023).
He, T., Cheng, X. & Xing, C. The gut microbial diversity of colon cancer patients and the clinical significance. Bioengineered 12, 7046–7060 (2021).
Ai, D. et al. Identifying gut microbiota associated with colorectal cancer using a zero-inflated lognormal model. Front. Microbiol. 10, 826 (2019).
Chen, W. et al. Enhanced microbiota profiling in patients with quiescent Crohn’s disease through comparison with paired healthy first-degree relatives. Cell Rep. Med. 5, 101624 (2024).
Liu, D. et al. Anaerostipes hadrus, a butyrate-producing bacterium capable of metabolizing 5-fluorouracil. mSphere 9, e0081623 (2024).
Ihekweazu, F. D. et al. Bacteroides ovatus ATCC 8483 monotherapy is superior to traditional fecal transplant and multi-strain bacteriotherapy in a murine colitis model. Gut Microbes 10, 504–520 (2019).
Ihekweazu, F. D. et al. Bacteroides ovatus promotes IL-22 production and reduces trinitrobenzene sulfonic acid-driven colonic inflammation. Am. J. Pathol. 191, 704–719 (2021).
Hayase, E. et al. Bacteroides ovatus alleviates dysbiotic microbiota-induced graft-versus-host disease. Cell Host Microbe 32, 1621–1636.e6 (2024).
Liu, N. et al. Eubacterium rectale Improves the efficacy of anti-PD1 immunotherapy in melanoma via l-serine-mediated NK cell activation. Research (Washington, DC) 6, 0127 (2023).
Lu, H. et al. Butyrate-producing Eubacterium rectale suppresses lymphomagenesis by alleviating the TNF-induced TLR4/MyD88/NF-κB axis. Cell Host Microbe 30, 1139–1150.e7 (2022).
Marietta, E. V. et al. Suppression of inflammatory arthritis by human gut-derived Prevotella histicola in humanized mice. Arthritis Rheumatol. 68, 2878–2888 (2016).
Shahi, S. K. et al. Prevotella histicola, a human gut commensal, is as potent as COPAXONE® in an animal model of multiple sclerosis. Front. Immunol. 10, 462 (2019).
Qiu, X., Zhang, M., Yang, X., Hong, N. & Yu, C. Faecalibacterium prausnitzii upregulates regulatory T cells and anti-inflammatory cytokines in treating TNBS-induced colitis. J. Crohns Colitis 7, e558–e568 (2013).
Martín, R. et al. The commensal bacterium Faecalibacterium prausnitzii is protective in DNBS-induced chronic moderate and severe colitis models. Inflamm. Bowel Dis. 20, 417–430 (2014).
Arpaia, N. et al. Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation. Nature 504, 451–455 (2013).
Aktas, B., Aslim, B. & Ozdemir, D. A. A neurotherapeutic approach with Lacticaseibacillus rhamnosus E9 on gut microbiota and intestinal barrier in MPTP-induced mouse model of Parkinson’s disease. Sci. Rep. 14, 15460 (2024).
Liu, X. et al. Polymannuronic acid prebiotic plus Lacticaseibacillus rhamnosus GG probiotic as a novel synbiotic promoted their separate neuroprotection against Parkinson’s disease. Food Res. Int. 155, 111067 (2022).
Liao, J.-F. et al. Lactobacillus plantarum PS128 alleviates neurodegenerative progression in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse models of Parkinson’s disease. Brain Behav. Immun. 90, 26–46 (2020).
Lee, Y. Z. et al. Neuroprotective effects of Lactobacillus plantarum PS128 in a mouse model of Parkinson’s disease: the role of gut microbiota and microRNAs. Int. J. Mol. Sci. 24, 6794 (2023).
Qiao, C.-M. et al. Akkermansia muciniphila is beneficial to a mouse model of Parkinson’s disease, via alleviated neuroinflammation and promoted neurogenesis, with involvement of SCFAs. Brain Sci. 14, 238 (2024).
Lu, C.-S. et al. The add-on effect of Lactobacillus plantarum PS128 in patients with Parkinson’s disease: a pilot study. Front Nutr. 8, 650053 (2021).
Chu, C. et al. Meta-analysis of randomized controlled trials of the effects of probiotics in Parkinson’s disease. Food Funct. 14, 3406–3422 (2023).
Cheng, A. G. et al. Design, construction, and in vivo augmentation of a complex gut microbiome. Cell 185, 3617–3636.e19 (2022).
Han, S. et al. A metabolomics pipeline for the mechanistic interrogation of the gut microbiome. Nature 595, 415–420 (2021).
Rockenstein, E. et al. Differential neuropathological alterations in transgenic mice expressing α-synuclein from the platelet-derived growth factor and Thy-1 promoters. J. Neurosci. Res. 68, 568–578 (2002).
Fleming, S. M. et al. Early and progressive sensorimotor anomalies in mice overexpressing wild-type human alpha-synuclein. J. Neurosci. 24, 9434–9440 (2004).
Zhang, J. et al. Motor impairments, striatal degeneration, and altered dopamine–glutamate interplay in mice lacking PSD-95. J. Neurogenet. 28, 98–111 (2014).
Lewis, S. J. & Heaton, K. W. Stool form scale as a useful guide to intestinal transit time. Scand. J. Gastroenterol. 32, 920–924 (1997).
Nagakura, Y., Naitoh, Y., Kamato, T., Yamano, M. & Miyata, K. Compounds possessing 5-HT3 receptor antagonistic activity inhibit intestinal propulsion in mice. Eur. J. Pharm. 311, 67–72 (1996).
Camilleri, M. & Linden, D. R. Measurement of gastrointestinal and colonic motor functions in humans and animals. Cell. Mol. Gastroenterol. Hepatol. 2, 412–428 (2016).
Koslo, R. J., Burks, T. F. & Porreca, F. Centrally administered bombesin affects gastrointestinal transit and colonic bead expulsion through supraspinal mechanisms. J. Pharm. Exp. Ther. 238, 62–67 (1986).
Benjamini, Y. & Hochberg, Y. Controlling the false discovery rate: a practical and powerful approach to multiple testing. J. R. Stat. Soc. B: Stat. Methodol. 57, 289–300 (1995).
Cliff, N. Dominance statistics: ordinal analyses to answer ordinal questions. Psychol. Bull. 114, 494–509 (1993).
Efron, B. Better bootstrap confidence intervals. J. Am. Stat. Assoc. 82, 171–185 (1987).
Cochran, W. G. The combination of estimates from different experiments. Biometrics 10, 101–129 (1954).
Higgins, J. P. T. & Thompson, S. G. Quantifying heterogeneity in a meta-analysis. Stat. Med. 21, 1539–1558 (2002).
Lee, B. R. & Kamitani, T. Improved immunodetection of endogenous α-synuclein. PLoS ONE 6, e23939 (2011).
Dobin, A. et al. STAR: ultrafast universal RNA-seq aligner. Bioinformatics 29, 15–21 (2013).
Liao, Y., Smyth, G. K. & Shi, W. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. Bioinformatics 30, 923–930 (2014).
Love, M. I., Huber, W. & Anders, S. Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2. Genome Biol. 15, 550 (2014).
Yu, G., Wang, L.-G., Han, Y. & He, Q.-Y. clusterProfiler: an R package for comparing biological themes among gene clusters. OMICS 16, 284–287 (2012).
Wickham, H. Data analysis. In ggplot2: Elegant Graphics for Data Analysis (ed. Wickham, H.) 189–201 (Springer International Publishing, 2016).
Reynolds, M. C. et al. Delineating the drivers and functionality of methanogenic niches within an arid landfill. Appl. Environ. Microbiol. 88, e0243821 (2022).
Mohana Rangan, S. et al. Decoupling Fe0 application and bioaugmentation in space and time enables microbial reductive dechlorination of trichloroethene to ethene: evidence from soil columns. Environ. Sci. Technol. 57, 4167–4179 (2023).
Davis, T. L. et al. Chemical oxygen demand can be converted to gross energy for food items using a linear regression model. J. Nutr. 151, 445–453 (2021).
Dirks, B. et al. Methanogenesis associated with altered microbial production of short-chain fatty acids and human-host metabolizable energy. ISME J. 19, wraf103 (2025).
Corbin, K. D. et al. Host-diet-gut microbiome interactions influence human energy balance: a randomized clinical trial. Nat. Commun. 14, 3161 (2023).
Blanco-Míguez, A. et al. Extending and improving metagenomic taxonomic profiling with uncharacterized species using MetaPhlAn 4. Nat. Biotechnol. 41, 1633–1644 (2023).
Beghini, F. et al. Integrating taxonomic, functional, and strain-level profiling of diverse microbial communities with bioBakery 3. Elife 10, e65088 (2021).
Anderson, M. J. Permutational multivariate analysis of variance (PERMANOVA). In Wiley StatsRef: Statistics Reference Online (eds Balakrishnan, N. et al.) (John Wiley & Sons, 2017).
Nickols, W. A. et al. MaAsLin 3: refining and extending generalized multivariable linear models for meta-omic association discovery. Nat. Methods https://doi.org/10.1038/s41592-025-02923-9 (2026).
Baron, R. M. & Kenny, D. A. The moderator-mediator variable distinction in social psychological research: conceptual, strategic, and statistical considerations. J. Pers. Soc. Psychol. 51, 1173–1182 (1986).
King, G., Tomz, M. & Wittenberg, J. Making the most of statistical analyses: improving interpretation and presentation. Am. J. Political Sci. 44, 347–361 (2000).
Acknowledgements
The authors would like to thank the members of the Mazmanian laboratory for their helpful critiques and review of the manuscript. We thank T. Thron for husbandry and maintenance of the Thy1-ASO “Line 61” mouse line, and L.B. De los Santos, I. Cardenas, and J. Gutierrez for animal care. We are grateful to C. Oikonomou for manuscript editing and submission support, and Y. Garcia-Flores for lab administrative support. We would also like to thank J. Griffiths for help with tissue collections. Flow cytometric analysis was performed at the Caltech Flow Cytometry and Cell Sorting Facility, with support from M. Gregory. Multiplex analysis was done at the Caltech Protein Expression Center, with support from M. Anaya. RNA sequencing was carried out by the UCLA Technology Center for Genomics & Bioinformatics (TCGB). Metagenomics sequencing was made possible by Prebiomics S.r.l. (Trento, Italy), with support from M. Bolzan. Figures 1A, B and 2A were created in BioRender (Moiseyenko, A., 2025, https://BioRender.com/zvkyy6g, RRID: SCR_018361). This research was funded in part by Aligning Science Across Parkinson’s (ASAP-020495 and ASAP-000375) through the Michael J. Fox Foundation for Parkinson’s Research (MJFF) and the Heritage Medical Research Institute to S.K.M., as well as by the Jacobs Institute for Molecular Engineering for Medicine (Caltech) and Beckman Institute at Caltech to R.F.I. For the purpose of open access, the authors have applied a CC BY public copyright license to all Author Accepted Manuscripts arising from this submission.
Author information
Authors and Affiliations
Contributions
A.M. and S.K.M. designed the studies and wrote the manuscript. A.M. led all investigations and drafted figures. Metagenomic analysis and figure creation were executed by G.A., while data processing was done by K.L., with supervision from N.S. and L.D.W. A.M.S. assisted with flow cytometry experiments, tissue collections, and initial manuscript editing. J.C.B. carried out downstream RNA sequencing analysis and figure creation for this data. B.D. collected volatile fatty acid measurements with assistance from D.D., and supervision from R.K.B. A.D.O. performed statistical analysis for motor and GI function assays. A.V.W. supported the design and quality control of RNA sequencing methodology and raw data processing, with supervision from R.F.I. P.S. assisted with behavior data collection and tissue collections. All authors read and approved the final manuscript.
Corresponding authors
Ethics declarations
Competing interests
S.K.M. is a founder and board member of Vertero Therapeutics and has equity in Nuanced Health and Seed Health. A.M. and S.K.M. hold a patent (US20240066074A1) on the use of Faecalibacterium prausnitzii and Prevotella histicola for the treatment of PD and have a pending application (US patent application 63/883,383) for the use of Faecalibacterium prausnitzii as a treatment for PD. The other authors do not have a competing interest.
Additional information
Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Supplementary information
Rights and permissions
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
About this article
Cite this article
Moiseyenko, A., Antonello, G., Schonhoff, A.M. et al. Faecalibacterium prausnitzii, depleted in the Parkinson’s disease microbiome, improves motor deficits in α-synuclein overexpressing mice. npj Parkinsons Dis. (2026). https://doi.org/10.1038/s41531-026-01287-x
Received:
Accepted:
Published:
DOI: https://doi.org/10.1038/s41531-026-01287-x


