{
  "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.",
  "abstract_shown": true,
  "affiliations": [
    "Department of Environmental Health Sciences, University of Georgia, Athens, GA 30605, USA"
  ],
  "article_type": null,
  "arxiv": null,
  "author_total": 2,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Ali Rehman"
    },
    {
      "affs": [
        0
      ],
      "name": "Lili Tang",
      "orcid": "0000-0001-5595-2875"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/dbza0mqwfpyck.bib",
  "cited_by": 0,
  "doi": "10.3390/nu18203304",
  "fulltext_url": null,
  "id": "dbza0mqwfpyck",
  "issns": [
    "2072-6643"
  ],
  "landing_url": "https://www.mdpi.com/2072-6643/18/20/3304",
  "language": null,
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "openalex",
      "2728|Parkinson's Disease Mechanisms and Treatments"
    ]
  ],
  "openalex": "W7221130025",
  "pdf_url": null,
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-09",
  "publisher": "MDPI AG",
  "ris": "https://research.draconitic.com/paper/dbza0mqwfpyck.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:19:56Z",
      "native_id": "10.3390/nu18203304",
      "source": "crossref",
      "url": "https://www.mdpi.com/2072-6643/18/20/3304"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2728|Parkinson's Disease Mechanisms and Treatments",
      "subfield": "neurology"
    }
  ],
  "title": "From Tea Catechins to Microbial Metabolites: Emerging Mechanisms for Modulating Gut-Origin α-Synuclein Seeding in Parkinson’s Disease",
  "title_text": "From Tea Catechins to Microbial Metabolites: Emerging Mechanisms for Modulating Gut-Origin α-Synuclein Seeding in Parkinson’s Disease",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:19:56Z",
  "url": "https://research.draconitic.com/paper/dbza0mqwfpyck",
  "venue": "Nutrients",
  "versions": []
}