Gut Bacteria Seems Different in Early Parkinson’s Patients

By the time Parkinson’s patients begin experiencing the disease’s hallmark symptoms, such as tremors or muscle rigidity, the disease has run rampant for decades and portions of the brain have already been irreversibly destroyed.

While searching for an early warning sign of the disease, researchers at the University of Luxembourg may have found one in the gut: They have discovered that the bacterial community in the gut of Parkinson’s patients differs from that of healthy people even at a very early stage.

Experts on Parkinson’s have long been discussing the idea that the disease begins to develop far outside the brain. According to the “dual hit” hypothesis, a hitherto unknown pathogen intrudes into the body through two points of entry: the nose or the gastrointestinal tract.

Once there, the pathogen sets the disease in motion, above all leading to the misfolding of the protein alpha-synuclein. This is a protein presumed to be involved in the excretion of messengers such as dopamine.

The misfolding of this protein could spread through the nerve pathways, where decades later it results in the typical clumping in the dopaminergic cells, known as Lewy bodies, that are characteristic of Parkinson’s. Ultimately, nerve cells start to die off and the hallmark symptoms of Parkinson’s appear.

The researchers, led by Professor Paul Wilmes, head of the Eco-Systems Biology Group at the Luxembourg Centre for Systems Biomedicine (LCSB) at the University of Luxembourg, wanted to investigate whether the early events in the course of the disease change the bacterial community, or the microbiome, at the two possible ports of entry.

They took samples from the nose and gut of 76 Parkinson’s patients and 78 healthy controls. They also examined the microbiome of 21 people diagnosed with idiopathic rapid-eye-movement sleep behavior disorder (iRBD). People with this sleep disorder have a much greater risk of developing Parkinson’s disease later in life.

The findings revealed that the bacterial community of the gut differed considerably between all three groups.

“Parkinson’s patients could be differentiated from healthy controls by their respective gut bacteria,” said first author Dr. Anna Heintz-Buschart from the Eco-Systems Biology Group.

In addition, the majority of the differential bacteria showed similar trends in the iRBD group. For example, certain germs were more common in one group while less common in others.

However, the researchers found no such differences in the samples from the subjects’ nasal cavities. The findings also showed that certain gut microbes are associated with non-motor Parkinson’s symptoms, such as depression.

“We hope that, by comparing the groups, we will learn to better understand the role of the microbiome in the process of the disease and to find out what changes occur and when,” said Wilmes.

“This might deliver new starting points for early treatment of the disease. It would also be essential knowledge for one day being able to use the absence or presence of certain bacteria as a biomarker for early detection of the disease.”

The researchers published their findings in the scientific journal Movement Disorders.

Source: University of Luxembourg

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