Gut bacteria composition in animal models of Parkinson’s disease: a systematic review and meta-analysis

Publication date

2026-01-27

Authors

Elford, Joshua D.ORCID 0000-0001-7336-2967ISNI 0000000518165337
Heesbeen, Elise JasmijnORCID 0000-0001-8213-7657ISNI 0000000512534496
van der Plaats, Nienke A.
Garssen, J.ORCID 0000-0002-8678-9182ISNI 0000000034097251
Kraneveld, Aletta D.ISNI 000000038803088X
Groenink, LucianneORCID 0000-0002-4971-7796ISNI 0000000394881736
Perez Pardo, PaulaISNI 0000000396807038

Editors

Advisors

Supervisors

Document Type

Article
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License

cc_by_nc_nd

Abstract

The gut microbiome is believed to play an important role in the development and onset of Parkinson’s disease (PD). While human studies report differences in gut microbiota between PD individuals and healthy controls, it is unclear whether preclinical animal models show similar patterns. We performed a systematic review and Bayesian regularised meta-analysis of preclinical PD studies that assessed both motor function and gut microbiota. Motor deficits were consistently observed across models, but gut bacterial diversity (α-diversity) and changes in key taxa (e.g. Akkermansia, Lactobacillus, Bifidobacterium) were inconsistent and poorly aligned with human data. In contrast, short-chain fatty acids (SCFAs) showed more reproducible changes and greater translatability to human findings. Chronic toxin-based models demonstrated the highest reproducibility. Overall, gut microbiota composition in animal PD models lacks consistency and human relevance, whereas SCFAs may offer a more reliable outcome. Finally, our study makes possible recommendations for reporting to improve future studies.

Keywords

Neurology, Clinical Neurology, Cellular and Molecular Neuroscience, SDG 3 - Good Health and Well-being

Citation

Elford, J D, Heesbeen, E J, van der Plaats, N A, Garssen, J, Kraneveld, A D, Groenink, L & Perez Pardo, P 2026, 'Gut bacteria composition in animal models of Parkinson’s disease : a systematic review and meta-analysis', npj Parkinson's Disease, vol. 12, no. 1, 31. https://doi.org/10.1038/s41531-025-01236-0