A group of scientists from University of Helsinki and University of Finland Oriental discovered a curious relationship between the development of Parkinson’s disease and the presence in the body of bacteria typical of wet and swampy environments.
This is an interesting discovery because this bacterium can become Diana prevent the development of symptoms of Parkinson’s disease or at least slow them down. However, it is too early to do so. First, further work needs to be done to demonstrate the role of the bacterium. Desulfofibrion in the progression of the disease.
So far this has been done in two ways. On the one hand, analysis of the faeces of patients with Parkinson’s disease in search of bacteria. On the other hand, feeding these bacteria to a group genetically modified worms for the development of the disease. Thus, significant evidence was found, as the authors point out in a study published in Borders of cellular and infectious microbiology. But we still have to work on it.
Pseudo-gut brain
It is often said that the gut is our second brain. But this is not true. At least if we are strict. It is true that it contains neurons, but in much smaller quantities than in the brain. In addition, the intestine forms much simpler structures than complex ones. brain networks.
On the other hand, it is true that the gut releases serotonin, which acts as a neurotransmitter in nerve cells. But in this case, its function is completely different, since it is responsible for promoting peristaltic movements, facilitating the passage of the food bolus through the intestines. For these and many other reasons, we cannot say that the gut is our second brain. But it is true that, according to some studies, there is a definite connection between gut microbiota and the development of certain neurological diseases. That is, the composition of the populations of bacteria living in our intestines can affect the health of our brain.
It has been studied in diseases such as multiple sclerosis, the origin of which is really autoimmune. But it has also been observed in other purely neurological diseases, such as Parkinson’s disease.
Paper Desulfofibrion in Parkinson’s disease
Desulfofibrion a genus of bacteria that normally live in aquatic environments with a high content of organic mattersuch as marshes or wetlands. However, they have also been found in the human intestine and are more present in patients with Parkinson’s disease.
This discovery prompted a group of Finnish scientists to dig further. For this, they participated 10 Parkinson’s patients and their healthy partners. Fecal samples were taken from all of them in order to later isolate the bacteria that make up them.
Then they fed them to a row of worms. Caenorhabditis elegans genetically modified to express a protein gene human alpha synuclein. This protein was chosen because it is strongly associated with Parkinson’s disease. It is known that this disease is characterized by the accumulation in certain parts of the brain of structures called Lewy bodies. They are mainly composed of α-synuclein, a protein that plays a very important role in the release of neurotransmitters, which are essential substances for the transmission of nerve signals through neurons. Therefore, it was important that the worms used as models could synthesize the human version of this protein.
And there was the key. When the worms were fed Desulfofibrion isolated from the faeces of patients with Parkinson’s disease, an increase in the synthesis of α-synuclein was observed in their brain cells. On the other hand, although the bacterium was found in some pairs of patients when they were fed worms. protein synthesis did not increase.
Logically, there is a big difference between a worm and a human. However, it must be taken into account that S. elegans widely used in research precisely because it shares many genes and molecular pathways with us. This indicates that the results of the study are highly relevant, but also that there is still much to be explored. At least we already know the possible culprit of Parkinson’s disease. Now it’s time to continue pulling the thread.
Source: Hiper Textual
