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0 reviewsParkinson’s disease (PD) is characterized by the selective degeneration of1234567890():,;1234567890():,;midbrain dopaminergic neurons and aggregation of α-synuclein. Emergingevidence implicates the gut microbiome in PD, with microbial metabolitesproposed as potential pathological mediators. However, the specific microbesand metabolites involved, and whether gut-derived metabolites can reach thebrain to directly induce neurodegeneration, remain unclear. Here we showthat elevated levels of Streptococcus mutans (S. mutans) and its enzyme urocanate reductase (UrdA), which produces imidazole propionate (ImP), in thegut microbiome of patients with PD, along with increased plasma ImP. Colonization of mice with S. mutans harboring UrdA or Escherichia coli expressingUrdA from S. mutans increases systemic and brain ImP levels, inducing PD-likesymptoms including dopaminergic neuronal loss, astrogliosis, microgliosis,and motor impairment. Additionally, S. mutans exacerbates α-synucleinpathology in a mouse model. ImP administration alone recapitulates key PDfeatures, supporting the UrdA–ImP axis as a microbial driver of PD pathology.Mechanistically, mTORC1 activation is crucial for both S. mutans- and ImPinduced PD pathology. Together, these findings identify microbial ImP, produced via UrdA, as a direct pathological mediator of the gut-brain axis in PD.
