From Tea Catechins to Microbial Metabolites: Emerging Mechanisms for Modulating Gut-Origin α-Synuclein Seeding in Parkinson’s Disease
- 1Department of Environmental Health Sciences, University of Georgia, Athens, GA 30605, USA
Abstract
Parkinson’s disease (PD) is increasingly recognized as a heterogeneous neurodegenerative disorder with multiple clinical and pathological trajectories. In a subset of patients, α-synuclein pathology may begin in the gut and subsequently spread to the brain, a pathway most relevant to the proposed body-first subtype of PD. Tea catechins, particularly epigallocatechin-3-gallate (EGCG), can influence α-synuclein aggregation, oxidative stress, inflammatory signaling, and gut microbial ecology. Because their systemic bioavailability is limited, substantial amounts reach the intestine and undergo microbiota-dependent biotransformation. This review examines whether parent catechins and their microbial metabolites could modify intestinal processes relevant to α-synuclein misfolding and seeding. Evidence indicates that catechins are converted into phenyl-γ-valerolactones and lower-molecular-weight phenolic metabolites, while microbial amyloids such as curli can promote α-synuclein aggregation in experimental models. EGCG can also remodel α-synuclein assemblies, and catechin exposure can alter microbial and inflammatory phenotypes. However, direct evidence that catechin-derived microbial metabolites inhibit curli–α-synuclein cross-seeding or reduce enteric α-synuclein seeding remains limited. By distinguishing general neuroprotection from effects on aggregation, seeding, and disease modification, this review integrates current evidence and highlights the potential relevance of microbiota-dependent catechin metabolism to gut-origin α-synuclein pathology and body-first PD.
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BibTeX
@article{rehman2026from,
title = {{From Tea Catechins to Microbial Metabolites: Emerging Mechanisms for Modulating Gut-Origin α-Synuclein Seeding in Parkinson’s Disease}},
author = {Ali Rehman and Lili Tang},
journal = {Nutrients},
year = {2026},
month = oct,
doi = {10.3390/nu18203304},
url = {https://www.mdpi.com/2072-6643/18/20/3304},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - From Tea Catechins to Microbial Metabolites: Emerging Mechanisms for Modulating Gut-Origin α-Synuclein Seeding in Parkinson’s Disease
AU - Ali Rehman
AU - Lili Tang
PY - 2026
DA - 2026/10/09
JO - Nutrients
DO - 10.3390/nu18203304
UR - https://www.mdpi.com/2072-6643/18/20/3304
AB - Parkinson’s disease (PD) is increasingly recognized as a heterogeneous neurodegenerative disorder with multiple clinical and pathological trajectories. In a subset of patients, α-synuclein pathology may begin in the gut and subsequently spread to the brain, a pathway most relevant to the proposed body-first subtype of PD. Tea catechins, particularly epigallocatechin-3-gallate (EGCG), can influence α-synuclein aggregation, oxidative stress, inflammatory signaling, and gut microbial ecology. Because their systemic bioavailability is limited, substantial amounts reach the intestine and undergo microbiota-dependent biotransformation. This review examines whether parent catechins and their microbial metabolites could modify intestinal processes relevant to α-synuclein misfolding and seeding. Evidence indicates that catechins are converted into phenyl-γ-valerolactones and lower-molecular-weight phenolic metabolites, while microbial amyloids such as curli can promote α-synuclein aggregation in experimental models. EGCG can also remodel α-synuclein assemblies, and catechin exposure can alter microbial and inflammatory phenotypes. However, direct evidence that catechin-derived microbial metabolites inhibit curli–α-synuclein cross-seeding or reduce enteric α-synuclein seeding remains limited. By distinguishing general neuroprotection from effects on aggregation, seeding, and disease modification, this review integrates current evidence and highlights the potential relevance of microbiota-dependent catechin metabolism to gut-origin α-synuclein pathology and body-first PD.
SN - 2072-6643
ER -