Dietary administration of the marine bacterium Stutzerimonas stutzeri protects against dopaminergic neuron loss, reduces α-synuclein levels, and improves motor and sensory phenotypes in C. elegans PD models via suppression of ferroptosis (restoring iron homeostasis, lowering lipid peroxidation, and…

Provides a mechanistically actionable lead—ferroptosis modulation by a marine-derived microbe—with biomarker readouts and clear neuroprotective effects in vivo, offering a promising source of bioactive compounds for PD drug discovery that warrants validation in mammalian models.

Parkinson's disease (PD) is a rapidly escalating neurodegenerative disorder marked by dopaminergic neurodegeneration, α-synuclein aggregation, and motor and non-motor impairments. Current therapies largely provide symptomatic relief and fail to prevent disease progression, underscoring the need for novel disease-modifying strategies. The marine biome has emerged as an unexplored reservoir of bioactive metabolites with neuroprotective potential, yet their therapeutic relevance in PD remains incompletely explored. Here, we report that Stutzerimonas stutzeri, a marine bacterium isolated from the Gulf of Mannar, exerts robust neuroprotective effects in Caenorhabditis elegans PD models. Dietary administration of S. stutzeri rescued dopaminergic neuronal loss, mitigated α-synuclein expression, and improved motor and sensory phenotypes. Mechanistic analyses revealed suppression of ferroptosis, evidenced by restoration of iron homeostasis, attenuation of lipid peroxidation, and recovery of ftn-1 expression. Our findings establish S. stutzeri as a previously unrecognized marine-derived therapeutic prospect for PD intervention and highlight ferroptosis modulation as a tractable therapeutic axis in neurodegeneration.