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<p>Parkinson’s disease is a common neurodegenerative disease related to both genetic and environmental insults. Epidemiological studies have linked <i>Helicobacter pylori (H. pylori</i>) infection to Parkinson’s disease risk, but the underlying mechanisms of this association remain unclear. In this study, we investigated whether chronic infection with a pathogenic <i>H. pylori</i> strain could induce α-synuclein aggregation or neurodegeneration, and whether infection clearance mitigates these effects. We also assessed whether <i>H. pylori</i> infection exacerbates α-synuclein pathology and neuron loss when combined with seeding of α-synuclein pathology. We find that chronic <i>H. pylori</i> infection induces a sustained immune response in the gut and plasma that leads to mild brain inflammation and dopaminergic neuron loss, independent of α-synuclein pathology. These effects are attenuated by eradication of the infection. In mice with α-synuclein pathology induced by pre-formed fibrils, <i>H. pylori</i> does not further exacerbate the extent of pathology or neuronal death. Together, these results suggest that <i>H. pylori</i> infection can lead to neurodegeneration through inflammatory mechanisms independent of α-synuclein aggregation. Our findings offer mechanistic insights into how pathogens could influence the risk and progression of Parkinson’s disease.</p>

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Helicobacter pylori infection and α-synuclein pathology drive parallel neurodegenerative pathways in the substantia nigra

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月22日

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  • Alejandro Soto-Avellaneda,
  • Alice Prigent,
  • Lindsay Meyerdirk,
  • Noah Schautz,
  • John Andrew Pospisilik,
  • Lena Brundin,
  • Michael X. Henderson

摘要

Parkinson’s disease is a common neurodegenerative disease related to both genetic and environmental insults. Epidemiological studies have linked Helicobacter pylori (H. pylori) infection to Parkinson’s disease risk, but the underlying mechanisms of this association remain unclear. In this study, we investigated whether chronic infection with a pathogenic H. pylori strain could induce α-synuclein aggregation or neurodegeneration, and whether infection clearance mitigates these effects. We also assessed whether H. pylori infection exacerbates α-synuclein pathology and neuron loss when combined with seeding of α-synuclein pathology. We find that chronic H. pylori infection induces a sustained immune response in the gut and plasma that leads to mild brain inflammation and dopaminergic neuron loss, independent of α-synuclein pathology. These effects are attenuated by eradication of the infection. In mice with α-synuclein pathology induced by pre-formed fibrils, H. pylori does not further exacerbate the extent of pathology or neuronal death. Together, these results suggest that H. pylori infection can lead to neurodegeneration through inflammatory mechanisms independent of α-synuclein aggregation. Our findings offer mechanistic insights into how pathogens could influence the risk and progression of Parkinson’s disease.