Anyone that has experience dealing with Parkinson’s disease (or knows someone that does) knows just how sneaky and vile this disease can be. The disease is well-known for causing motor dysfunctions, muscle rigidity, tremors, and other debilitating symptoms. This leads to the victim feeling “stuck” in their own body.
Unfortunately, there is no cure for the disease, and it grows steadily worse over time.
Research now tells us that Parkinson’s begins to form far outside the brain. According to the “dual hit” theory, an unknown pathogen sneaks into the body through either the GI tract or the nose. According to Medical News Today:
Once there, it sets a pathological process in motion, above all the misfolding of the protein alpha-synuclein. This is a protein whose exact function remains unknown. Among other things, it is presumed to be involved in the excretion of messengers such as dopamine. The misfolding of this protein could propagate through the nerve pathways, where – decades later – it produces 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 typical symptoms of Parkinson’s disease appear.
Unfortunately, once the physical symptoms of the disease appear, portions of the brain have already become destroyed, and the effects are irreversible. At this point, it is clear that the disease began decades earlier.
Researchers at at the University of Luxembourg have been working hard to discover more about this disease, and how it comes into the body. Through their research, they have made a discovery: the bacterial community existing in the gut of Parkinson’s patients is different from the bacterial community existing in the gut of healthy people. This is the case even in the earliest stages of the disease.
They found this information by taking bacterial samples from the nose and gut of 76 Parkinson’s patients, as well as from 78 healthy individuals. They also took samples from 21 individuals who had a diagnosis of iRBD (Idiopathic Rapid-Eye-Movement Sleep Behaviour Disorder), since people with this sleep disorder have a much greater risk of developing Parkinson’s disease.
Through this study, the researchers made the discovery that the gut bacterial community was different among all three groups. As the study states:
“Parkinson’s patients could be differentiated from healthy controls by their respective gut bacteria,” explains the first author Dr. Anna Heintz-Buschart from the Eco-Systems Biology Group. And the majority of the differential bacteria showed similar trends in the iRBD group. For example, certain germs were more prevalent in one group while the count was lower in others. In the samples from the subjects’ nasal cavities, however, the researchers found no such differences. The study also revealed that certain gut microbes are associated with non-motor Parkinson’s symptoms, for example depression.
By further comparing these three groups, the researchers hope to discover more about the bacterial community residing in Parkinson’s patients, and to further understand what changes occur (and when) throughout the progression of the disease.