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A common bacterium could be among the causes of Parkinson’s disease

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A common genus of microbe found in wet, swampy environments could play a key role in the development of Parkinson’s disease by excreting compounds that trigger the formation of toxic clumps of proteins inside brain cells.

The discoveries, made by a small group of researchers from the University of Helsinki and the University of Eastern Finland, are based on the results of a previous investigation which showed 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 genetically engineered worms to the physical changes in the brain that coincide with Parkinson’s disease, the researchers hope to one day improve early detection of the disease in humans, or even slow its progress.

‘Our results make it possible to identify carriers of these harmful Desulfovibrio bacteria,’ explains senior author Per Saris, a microbiologist at the University of Helsinki in Finland.

“As a result, they can be targeted with measures to remove these stumps from the gut, potentially relieving and slowing the symptoms of Parkinson’s disease patients.”

Ever since British physician James Parkinson first described the disease as a neurological condition nearly two centuries ago, researchers have sought an explanation for why some people develop a dramatic loss of fine motor control as they age.

Physiologically, small inclusions known as Lewy bodies accumulate in cells in specific regions of the brain of individuals diagnosed with Parkinson’s disease.

More recently, investigations of these microscopic clumps of material have revealed that they are largely made up of a type of protein called α-synuclein, which is typically involved in the release of neurotransmitters.

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It is not yet fully understood how this clump contributes to Parkinson’s pathology, although it is suspected that the very presence of these concentrations, called protofibrils, is not positive for the healthy functioning of nerve cells.

Another mystery is the initial cause of α-synuclein aggregation. Although Parkinson’s can run in families, genetics appear to explain only 10-15% of all cases.

That leaves environmental conditions as a likely suspect, with studies finding that the types of bacteria we harbor in our gut predict the likelihood of an individual having, or at least developing, Parkinson’s symptoms.

With Saris’ 2021 study, it was finally shown that there is a single main suspect that researchers can focus on.

“The disease is mainly caused by environmental factors, that is, environmental exposure to the Desulfovibrio bacterial strains that cause Parkinson’s,” says Saris.

In the new study, Saris and his team took fecal samples from 10 Parkinson’s patients and their healthy spouses and isolated the strains of Desulfovibrio present.

Together with two control groups of bacteria belonging to an entirely different genus, the extracted microbes were then administered to transgenic specimens of the nematode Caenorhabditis elegans, modified to express human α-synuclein.

A statistical analysis based on microscopic observation of nematode heads revealed that those fed Desulfovibrio were indeed much more likely to produce clumps of α-synuclein, and that these clumps were much larger.

Interestingly, strains of Desulfovibrio taken from Parkinson’s patients were also able to aggregate proteins in C. elegans better than those taken from their partners.

Furthermore, these worms died in higher numbers than those in the control groups.

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Of course, there is a big difference between worms and humans. While the same experiment can never be replicated in a sample of healthy people, studies will continue to look closely at the ways in which Desulfovibrio in our gut might trigger the formation of α-synuclein aggregates that could migrate through the body. .

Over time, we may also be able to manage the course of Parkinson’s disease by using therapies that target the digestive system and surrounding nerves, instead of the brain.

“Once Desulfovibrio bacteria are cleared from the gut, α-synuclein aggregates are no longer formed in the intestinal cells, from where they travel to the brain via the vagus nerve like prion proteins,” suggests Saris.

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