# Gut microbiota and Parkinson’s disease: exploring pathogenesis and potential therapeutic strategies from a gut-brain axis perspective

**Authors:** Xiayu Jin, Jirui Wei, Xudong Min, Yiqi Fan, Zhao Yuan, Zhuolin Du, Zequn Su, Tianrong Xun, Qingyao Du, Tiecheng Liang, Xiaozheng He, Waijiao Tang

PMC · DOI: 10.1016/j.isci.2025.114185 · iScience · 2025-12-04

## TL;DR

This review explores how the gut microbiota influences Parkinson’s disease and highlights potential gut-targeted therapies for treatment.

## Contribution

The paper systematically summarizes the gut’s role in PD pathogenesis and novel therapeutic strategies from a gut-brain axis perspective.

## Key findings

- The gut microbiota contributes to PD through mechanisms like neuroinflammation and α-synuclein aggregation.
- Gut-targeted therapies such as FMT and SCFA supplementation show promise for PD treatment.
- Understanding gut-brain interactions may improve early diagnosis and treatment of PD.

## Abstract

Parkinson’s disease (PD) is a prevalent neurodegenerative disorder with a global prevalence exceeding 1‰, posing a significant public health challenge. Although the pathogenesis of PD is not yet fully elucidated, accumulating evidence suggests that it results from the interplay between genetic and environmental factors, highlighting its multifactorial nature. With advances in translational medicine, the gut has emerged as a critical participant in PD onset and progression. This review systematically summarizes the role of the gut in PD, particularly emphasizing potential mechanisms involving neuroinflammation in the central nervous system (CNS), pathological aggregation of α-synuclein (α-syn), and mitochondrial dysfunction. Furthermore, gut-targeted therapeutic strategies for PD are discussed, including fecal microbiota transplantation (FMT), gut-directed anti-inflammatory therapies, supplementation with gut microbiota-derived metabolites such as short-chain fatty acids (SCFAs), and interventions targeting α-syn aggregation. A deeper understanding of these mechanisms not only advances the pathological knowledge of PD but also provides theoretical foundations for the early diagnosis and innovative treatment of the disease.

Neuroscience; Microbiology

## Linked entities

- **Diseases:** Parkinson’s disease (MONDO:0005180)

## Full-text entities

- **Genes:** SNCA (synuclein alpha) [NCBI Gene 6622] {aka NACP, PARK1, PARK4, PD1}
- **Diseases:** inflammatory (MESH:D007249), PD (MESH:D010300), mitochondrial dysfunction (MESH:D028361), neurodegenerative disorder (MESH:D019636), neuroinflammation (MESH:D000090862)
- **Chemicals:** SCFAs (MESH:D005232)

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12830195/full.md

## References

250 references — full list in the complete paper: https://tomesphere.com/paper/PMC12830195/full.md

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Source: https://tomesphere.com/paper/PMC12830195