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

Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by the demise of dopaminergic (DA) neurons and the aggregation of alpha-synuclein, with ferroptosis playing a crucial role in its development. This research explored the neuroprotective properties of Kocuria rhizophila strain CDMP12, a marine bacterium sourced from the Gulf of Mannar, India, in Caenorhabditis elegans models of PD.

When K. rhizophila (CDMP12) was included in the diet, it not only preserved the structure of DA neurons but also rectified neuro-sensory and motor impairments, while simultaneously reducing alpha-synuclein expression in the C. elegans models. Through transcriptomic analysis and quantitative real-time PCR, the study uncovered that CDMP12 effectively curtailed ferroptosis by significantly downregulating iron and lipid regulatory genes like smf-3, ftn-1, and acs-4, while concurrently upregulating the antioxidant gene gpx-1.

Moreover, BODIPY staining indicated that treatment with CDMP12 led to a marked decrease in lipid peroxidation, thereby reducing the oxidized-to-non-oxidized lipid ratio in PD worms. In summary, these results suggest that K. rhizophila (CDMP12) is a promising marine-derived neuroprotective agent capable of mitigating PD-associated pathology, characterized by reduced alpha-synuclein levels, preservation of DA neuronal function, and attenuation of ferroptosis-linked molecular and lipid peroxidation patterns.