Marine bacterium Stutzerimonas stutzeri mitigates Parkinson's disease pathology in C. elegans via ferroptosis modulation.
Marine bacterium Stutzerimonas stutzeri mitigates Parkinson's disease pathology in C. elegans via ferroptosis modulation.
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
Lucknow, IN · Author affiliation
Division of Neuroscience and Ageing Biology, CSIR-Central Drug Research Institute, Lucknow, UP, India.Location evidence
Ghāziābād, IN · Author affiliation
Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, 201002, India.Location evidence
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Original abstract
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.