Strain-specific effects of Desulfovibrio on neurodegeneration and oxidative stress in a Caenorhabditis elegans PD model

Summary

This research shows that different strains of bacteria called Desulfovibrio have very different effects on brain health. When scientists exposed worms to six different strains, they found that environmental strains actually protected against Parkinson’s-like symptoms, while strains from human patients and animals caused more damage. The worms strongly preferred to eat the environmental strains, suggesting they could sense which bacteria were harmful. This highlights how the type of bacteria in our gut matters just as much as the total amount.

Background

The gut microbiota is increasingly recognized as a contributor to Parkinson’s disease (PD) pathology. Sulfate-reducing Desulfovibrio (DSV) bacteria have emerged as potential microbial drivers through production of hydrogen sulfide and other neurotoxic factors. However, strain-specific effects of these bacteria remain poorly characterized.

Objective

This study examined the strain-specific effects of six Desulfovibrio strains from human, animal, and environmental sources on food preference, alpha-synuclein aggregation, oxidative stress, gene expression, and lifespan in a C. elegans PD model expressing human α-synuclein.

Results

Environmental DSV strains, particularly D. vulgaris DSM 644, were strongly preferred by worms (94.7% preference) over human isolates. Animal and human-derived strains induced the highest α-synuclein aggregation and ROS production, while DSM 644 showed protective effects with minimal aggregation and extended lifespan (median 36 days). Strain-specific differences in stress-response gene expression correlated with pathological outcomes.

Conclusion

These findings demonstrate that DSV strains differentially influence neurodegeneration, oxidative stress, and aging in a strain-dependent manner, reinforcing the need for mechanistic validation in mammalian PD models and supporting the role of specific gut bacteria in Parkinson’s disease pathogenesis.
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