ORAL BACTERIA LINKED TO PARKINSON’S DISEASE THROUGH THE GUT–BRAIN AXIS: EVIDENCE OF STREPTOCOCCUS MUTANS METABOLITES AFFECTING NEURAL FUNCTION

Authors

  • Pedro Guimarães Sampaio Trajano dos Santos Author
  • Nadynne Eliza Maria de Lima Moura Author
  • Rosana Maria Coelho Travassos Author
  • Adriane Tenório Dourado Chaves Author
  • Josué Alves Author
  • Vanessa Lessa Cavalcanti de Araújo Author
  • Eliana Santos Lyra da Paz Author
  • Verônica Maria de Sá Rodrigues Author
  • Priscila Prosini Author
  • William Jose Lopes de Freitas Author
  • Lara Cardoso de Morais Author
  • Maria do Socorro Orestes Cardoso Author

DOI:

https://doi.org/10.56238/arev7n11-199

Keywords:

Parkinson’s Disease, Streptococcus Mutans, Gut–Brain Axis, Oral Microbiota, Neuronal Function, Imidazole Propionate

Abstract

Objective: This narrative review aims to analyze current evidence linking oral bacteria, particularly Streptococcus mutans, to Parkinson’s disease (PD) through the gut–brain axis (GBA). The focus is on microbial colonization of the intestine, metabolite production, and the mechanisms by which these metabolites influence neural function.

Methodology: A comprehensive search of PubMed, Scopus, Web of Science, and Google Scholar was conducted using the keywords “Streptococcus mutans,” “Parkinson’s disease,” “gut–brain axis,” “oral microbiota,” and “neuronal dysfunction.” Both in vivo and in vitro studies published in English between 2015 and 2025 were included.

Results: Evidence indicates that S. mutans can migrate to the intestine, producing urocanate reductase (UrdA) and its metabolite imidazole propionate (ImP), which enter systemic circulation and reach the brain. Animal models demonstrated that these metabolites contribute to dopaminergic neuron loss, neuroinflammation, motor dysfunction, and α-synuclein aggregation. The effects were mediated via activation of the mTORC1 signaling pathway, and pharmacological inhibition of mTORC1 mitigated neurodegenerative changes.

Conclusion: Oral bacteria, particularly S. mutans, may play a critical role in PD pathogenesis via the GBA. Targeting gut microbial composition and metabolite production represents a promising therapeutic avenue. The findings emphasize the potential importance of oral health in preventing or mitigating neurodegenerative disorders.

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References

Carabotti, M., Scirocco, A., Maselli, M. A., & Severi, C. (2015). The gut–brain axis: Interactions between enteric microbiota, central and enteric nervous systems. Annals of Gastroenterology, 28(2), 203–209. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367209/

Dauer, W., & Przedborski, S. (2003). Parkinson's disease: Mechanisms and models. Neuron, 39(6), 889–909. https://doi.org/10.1016/s0896-6273(03)00568-3

Heintz-Buschart, A., Pandey, U., Wicke, T., Sixel-Döring, F., Janzen, A., Sittig-Wiegand, E., ... & Wilmes, P. (2018). The nasal and gut microbiome in Parkinson’s disease. Movement Disorders, 33(1), 88–98. https://doi.org/10.1002/mds.27105

Kalia, L. V., & Lang, A. E. (2015). Parkinson’s disease. The Lancet, 386(9996), 896–912. https://doi.org/10.1016/S0140-6736(14)61393-3

Klein, C., & Westenberger, A. (2012). Genetics of Parkinson’s disease. Cold Spring Harbor Perspectives in Medicine, 2(1), a008888. https://doi.org/10.1101/cshperspect.a008888

Koh, A., Park, H., Lee, Y., Cheon, J., & Kim, H.-J. (2025). Oral bacteria linked to Parkinson’s disease via the gut–brain axis. Nature Communications, 14(1), 1234. https://doi.org/10.1038/s41467-025-63473-4

Scheperjans, F., Aho, V., Pereira, P. A. B., Koskinen, K., Paulin, L., Pekkonen, E., ... & Auvinen, P. (2015). Gut microbiota are related to Parkinson’s disease and clinical phenotype. Movement Disorders, 30(3), 350–358. https://doi.org/10.1002/mds.26069

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Published

2025-11-17

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Articles

How to Cite

SANTOS, Pedro Guimarães Sampaio Trajano dos et al. ORAL BACTERIA LINKED TO PARKINSON’S DISEASE THROUGH THE GUT–BRAIN AXIS: EVIDENCE OF STREPTOCOCCUS MUTANS METABOLITES AFFECTING NEURAL FUNCTION. ARACÊ , [S. l.], v. 7, n. 11, p. e10085, 2025. DOI: 10.56238/arev7n11-199. Disponível em: https://periodicos.newsciencepubl.com/arace/article/view/10085. Acesso em: 5 dec. 2025.