REVIEW: Role of the Gut Microbiome and Bacterial Amyloids in the Development of Synucleinopathies

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Nina P. Trubitsina¹, Anton B. Matiiv¹, Tatyana M. Rogoza^1,2, Anna A. Zudilova¹, Mariya D. Bezgina¹, Galina A. Zhouravleva^1,3, and Stanislav A. Bondarev^1,3,a,a*

¹Department of Genetics and Biotechnology, Saint Petersburg State University, 199034 Saint Petersburg, Russia

²St. Petersburg Branch of the Vavilov Institute of General Genetics, 198504 Saint Petersburg, Russia

³Laboratory of Amyloid Biology, Saint Petersburg State University, 199034 Saint Petersburg, Russia

Received September 18, 2023; Revised January 16, 2024; Accepted January 24, 2024

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Less than ten years ago, evidence began to accumulate about association between the changes in the composition of gut microbiota and development of human synucleinopathies, in particular sporadic form of Parkinson’s disease. We collected data from more than one hundred and thirty experimental studies that reported similar results and summarized the frequencies of detection of different groups of bacteria in these studies. It is important to note that it is extremely rare that a unidirectional change in the population of one or another group of microorganisms (only an elevation or only a reduction) was detected in the patients with Parkinson’s disease. However, we were able to identify several groups of bacteria that were overrepresented in the patients with Parkinson’s disease in the analyzed studies. There are various hypotheses about the molecular mechanisms that explain such relationships. Usually, α-synuclein aggregation is associated with the development of inflammatory processes that occur in response to the changes in the microbiome. However, experimental evidence is accumulating on the influence of bacterial proteins, including amyloids (curli), as well as various metabolites, on the α-synuclein aggregation. In the review, we provided up-to-date information about such examples.

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KEY WORDS: amyloids, alpha-synuclein, Parkinson’s disease, microbiome, dysbiosis, neurodegenerative diseases, bacterial amyloids, curli

DOI: 10.1134/S0006297924030118

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