Doitsidou Lab identify protective gut bacteria in a C. elegans Parkinson's model

Paper "Probiotic Bacillus subtilis Protects against α-Synuclein Aggregation in C. elegans" is now online on Cell Reports.


Graphical Abstract

Doitsidou Lab - Centre for Discovery Brain Sciences and colleagues from Dundee University have identified a probiotic – or so-called good bacteria – which prevents the build-up of a protein which is linked with Parkinson’s.   In people with Parkinson’s, alpha-synuclein protein builds up and forms toxic clumps which are associated with the death of dopamine producing nerve cells. The loss of dopamine is what causes motor symptoms in Parkinson’s. 

Using roundworms, scientists found that a probiotic called Bacillus subtilis could not only protect against the build-up of this protein, but can also clear some of the already formed protein clumps.

These new findings could pave the way for future studies that gauge how supplements such as probiotics impact Parkinson’s. 

The paper "Probiotic Bacillus subtilis Protects against α-Synuclein Aggregation in C. elegans" is now online on Cell Reports.


• B. subtilis PXN21 inhibits and reverses α-syn aggregation in a C. elegans model

• Spores and vegetative cells protect through different mechanisms

• The probiotic inhibits α-syn aggregation by changing the host sphingolipid metabolism

• Biofilm formation in the gut and bacterial metabolites reduce α-syn aggregation


Recent discoveries have implicated the gut microbiome in the progression and severity of Parkinson’s disease; however, how gut bacteria affect such neurodegenerative disorders remains unclear. Here, we report that the Bacillus subtilis probiotic strain PXN21 inhibits α-synuclein aggregation and clears preformed aggregates in an established Caenorhabditis elegans model of synucleinopathy. This protection is seen in young and aging animals and is partly mediated by DAF-16. Multiple B. subtilis strains trigger the protective effect via both spores and vegetative cells, partly due to a biofilm formation in the gut of the worms and the release of bacterial metabolites. We identify several host metabolic pathways differentially regulated in response to probiotic exposure, including sphingolipid metabolism. We further demonstrate functional roles of the sphingolipid metabolism genes lagr-1, asm-3, and sptl-3 in the anti-aggregation effect. Our findings provide a basis for exploring the disease-modifying potential of B. subtilis as a dietary supplement.

The results provide an opportunity to investigate how changing the bacteria that make up our gut microbiome affects Parkinson’s. The next steps are to confirm these results in mice, followed by fast-tracked clinical trials since the probiotic we tested is already commercially available.The quotation text is a mandatory field