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<p>Gut microbiome composition is altered in Parkinson’s disease (PD), the fastest-growing neurological condition, that is characterized by neurodegeneration, motor dysfunction, and is frequently accompanied by gastrointestinal (GI) symptoms. Notably, microbial taxa with anti-inflammatory properties are consistently depleted in PD patients compared to controls. To explore whether specific gut bacteria may be disease-protective, we assembled a microbial consortium of 8 human-associated taxa that are reduced in individuals with PD. Treatment of α-synuclein overexpressing (Thy1-ASO) mice, an animal model of PD, with this consortium improved motor and GI deficits. A single bacterial species from this consortium, <i>Faecalibacterium prausnitzii</i>, was sufficient to correct gut microbiome deviations in Thy1-ASO mice, induce anti-inflammatory immune responses, and promote protective colonic gene expression profiles. Accordingly, oral treatment with <i>F. prausnitzii</i> robustly ameliorated motor and GI deficits and reduced α-synuclein aggregates in the brain. These findings support the emerging hypothesis of functional contributions by the microbiome to PD outcomes, and embolden the development of potential probiotic therapies to treat motor and non-motor symptoms.</p>

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Faecalibacterium prausnitzii, depleted in the Parkinson’s disease microbiome, improves motor deficits in α-synuclein overexpressing mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月5日

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  • Anastasiya Moiseyenko,
  • Giacomo Antonello,
  • Aubrey M. Schonhoff,
  • Joseph C. Boktor,
  • Kaelyn Long,
  • Blake Dirks,
  • Anastasiya D. Oguienko,
  • Alexander Viloria Winnett,
  • Patrick Simpson,
  • Dorsa Daeizadeh,
  • Rustem F. Ismagilov,
  • Rosa Krajmalnik-Brown,
  • Nicola Segata,
  • Levi D. Waldron,
  • Sarkis K. Mazmanian

摘要

Gut microbiome composition is altered in Parkinson’s disease (PD), the fastest-growing neurological condition, that is characterized by neurodegeneration, motor dysfunction, and is frequently accompanied by gastrointestinal (GI) symptoms. Notably, microbial taxa with anti-inflammatory properties are consistently depleted in PD patients compared to controls. To explore whether specific gut bacteria may be disease-protective, we assembled a microbial consortium of 8 human-associated taxa that are reduced in individuals with PD. Treatment of α-synuclein overexpressing (Thy1-ASO) mice, an animal model of PD, with this consortium improved motor and GI deficits. A single bacterial species from this consortium, Faecalibacterium prausnitzii, was sufficient to correct gut microbiome deviations in Thy1-ASO mice, induce anti-inflammatory immune responses, and promote protective colonic gene expression profiles. Accordingly, oral treatment with F. prausnitzii robustly ameliorated motor and GI deficits and reduced α-synuclein aggregates in the brain. These findings support the emerging hypothesis of functional contributions by the microbiome to PD outcomes, and embolden the development of potential probiotic therapies to treat motor and non-motor symptoms.