A common genus of microbes found in wet, swampy environments may play a key role in the development of Parkinson's disease by excreting compounds that cause proteins inside brain cells to form toxic clumps.
The findings, by a team of researchers from the University of Helsinki and the University of Eastern Finland, build on the results of earlier research showing that the severity of the neurodegenerative disorder in volunteers increased with concentrations of bacterial strains of Desulfovibrio in their feces.
By now demonstrating a potential pathway from the presence of the bacteria in gene-edited worms to physical changes in the brain consistent with Parkinson's disease, the researchers hope to improve early diagnosis of the disease in humans, or even slow its progression.
"Our findings make it possible to detect carriers of these harmful Desulfovibrio bacteria. Consequently, they can be targeted for measures to eliminate these strains from the gut, potentially alleviating and slowing down the symptoms of Parkinson's disease patients," said microbiologist and lead author of the study, Per Saris.
The cause of this neurodegenerative disease is currently unknown for certain, and studies suggest that genetic factors are involved in only 10% to 15% of cases. Therefore, environmental factors could be one of the factors to be taken into account, even more so when it is known that accumulations of certain bacteria in our intestines correlate with the course of Parkinson's disease.
In the new research, the team took fecal samples from 10 Parkinson's patients and their healthy spouses, and isolated any strains of Desulfovibrio present. Along with two control groups of bacteria belonging to a completely different genus, the extracted test microbes were then administered to transgenic specimens of nematode Caenorhabditis elegans, which had been modified to express human α-synuclein. This is a protein that is often involved in the release of neurotransmitters in the diseased brain.
A statistical analysis based on microscopic observations of the nematode heads revealed that those fed Desulfovibrio were much more likely to produce clumps of the α-synuclein, and that these clumps were much larger.
Tellingly, strains of Desulfovibrio bacteria collected from Parkinson's patients were also better at aggregating proteins in C. elegans than those collected from their peers. What's more, those worms typically died in greater numbers than those in the control groups.
We may soon even be able to control the progression of the disease using therapies that target the digestive system and surrounding nerves, rather than the brain.
"Once the Desulfovibrio bacteria are eliminated from the gut, aggregates of α-synuclein stop forming in the intestinal cells, from where they travel to the brain via the vagus nerve, like prion proteins," Saris summarized.
