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bioRxiv · 10.64898/2026.08.25.746916

Mitigation of Parkinson's Disease Pathology in C. elegans by Marine Bacterium Kocuria rhizophila via Ferroptosis Suppression

VERMA, S.·Singh, S.·Damodaran, A.·Kumar, N.·Yadav, P.·Pasupuleti, M.
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Abstract

Parkinson's disease (PD) is a progressive neurodegenerative condition characterized by the loss of dopaminergic (DA) neurons and alpha-synuclein aggregation, with ferroptosis playing a critical pathological role. This study investigated the neuroprotective potential of Kocuria rhizophila strain CDMP12, a marine bacterium isolated from the Gulf of Mannar, India, using Caenorhabditis elegans models of PD. Dietary supplementation with K. rhizophila (CDMP12) significantly preserved DA neuron structure, rescued neuro-sensory and motor deficits, and attenuated both alpha-synuclein expression in the C. elegans models. Transcriptomic and qRT-PCR analyses revealed that CDMP12 systematically suppressed ferroptosis by significantly downregulating iron and lipid regulatory genes such as smf-3, ftn-1, and acs-4, while upregulating the protective antioxidant gene gpx-1. Furthermore, BODIPY staining demonstrated that CDMP12 treatment markedly reduced lipid peroxidation, lowering the oxidized-to-non-oxidized lipid ratio in PD worms. Collectively, these findings identify K. rhizophila (CDMP12) as a promising marine-derived neuroprotective candidate that mitigates PD-associated pathology, accompanied by reduced alpha-synuclein burden, preservation of DA neuronal function, and attenuation of ferroptosis-associated molecular and lipid peroxidation signatures.

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VERMA, S., Singh, S., Damodaran, A., Kumar, N., Yadav, P., Pasupuleti, M.. 2026-08-28. Mitigation of Parkinson's Disease Pathology in C. elegans by Marine Bacterium Kocuria rhizophila via Ferroptosis Suppression. https://doi.org/10.64898/2026.08.25.746916

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