Parkinson’s disease could be caused by a common aquatic bacterium: ScienceAlert

A common genus of microbe found in moist, swampy environments may play a key role in the development of Parkinson’s disease, by excreting compounds that trigger the formation of toxic masses in brain cells.

The findings, made by a small team of researchers from the University of Helsinki and the University of Eastern Finland, build on results from an earlier survey showing that the severity of neurodegenerative disease in volunteers increased with concentrations of Desulfovibrio bacterial strains in their faeces.

By now demonstrating a potential path from the bacteria’s presence in genetically modified worms to physical changes in the brain that coincide with Parkinson’s disease, researchers hope to one day improve early diagnosis of the disease in humans, or even slow down its progress.

“Our discoveries make it possible to detect the carriers of these harmful Desulfovibrio bacteria,” says lead author Per Saris, a microbiologist at the University of Helsinki in Finland.

“Therefore, they may be targeted with measures to eliminate these strains from the gut, potentially alleviating and slowing the symptoms of patients with Parkinson’s disease.”

Since English physician James Parkinson first described the disease as a neurological condition around two centuries ago, researchers have sought to explain why some people develop a drastic loss of fine motor control as they age.

Physiologically speaking, small inclusions called Lewy bodies accumulate in the cells of specific regions of the brain of people diagnosed with Parkinson’s disease.

More recently, research into these microscopic clumps of material has revealed that they consist largely of a type of protein called α-synuclein, which is typically involved in the release of neurotransmitters.

How this clumping contributes to the pathology of Parkinson’s disease is still not entirely clear, although it is suspected that the very presence of these concentrations, called protofibrils, may not be excellent for proper functioning. nerve cells.

What is also somewhat mysterious is the initial cause of α-synuclein aggregation. Although Parkinson’s disease can be inherited, genetics only seem to explain about 10-15% of all cases.

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

With Saris’ study in 2021, there was finally evidence of a single prime suspect that researchers could focus on.

“Disease is primarily caused by environmental factors, i.e. environmental exposure to Desulfovibrio bacterial strains that cause Parkinson’s disease,” says Saris.

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

With two different control groups of bacteria belonging to a completely different genus, the extracted test microbes were then fed transgenic samples of Caenorhabditis elegans nematode, which had been modified to express human α-synuclein.

Statistical analysis based on microscopic observations of nematode heads revealed those fed Desulfovibrio were indeed much more likely to produce α-synuclein clumps, and these clumps were more likely to be much larger.

Tellingly, Desulfovibrio strains collected from patients with Parkinson’s disease were also better at aggregating proteins in C.elegans than those collected from their partners.

Moreover, these worms generally die in greater numbers than those in the control groups.

Of course, there is a world of difference between worms and humans. Although the same experience may never be replicated in a sample of healthy people, studies will continue to look closely at ways Desulfovibrio in our own guts could trigger the formation of α-synuclein aggregates that could migrate through the body.

In time, we may even be able to manage the progression of Parkinson’s disease using therapies that target the digestive system and its surrounding nerves, rather than the brain.

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

This research was published in Frontiers in cellular and infectious microbiology.

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