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Can the microbiome predict Parkinson’s?

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The Gut microbiome influences many systems of the human body. Thus, it can create neurochemicals, such as serotonin, and communicate with the central nervous system. Furthermore, its relationship with the brain may influence dementia and autism.

In this sense, the authors of a new study focused on investigate the link between gut bacteria and Parkinson’s disease.

In this way, the team collected tissue samples from the appendix from people with Parkinson’s disease and a control group of people without the condition. The truth is that, although many people consider that the appendix has no biological function, there is growing scientific evidence that acts as a reservoir for gut microbes and alpha-synuclein, the characteristic protein of Parkinson’s.

Thus, as we have said before, the researchers collected samples of the appendix tissue, but also ileum and liver, which have an important role in the production of bile acids.

After someone eats, the substance is released in your intestines to help break down fats. Thus, bile salts are one of the key components of bile that helps break down these fats.

To study differences in microbial composition, the researchers compared the appendix microbiome of 12 people with Parkinson’s with 16 of the control group. In this way, they found that the appendages of people with the condition had higher levels of Peptostreptococcaceae, Lachonospiraceae and Burkholderialies.

In fact, burkholderia infects the brain. Some of the species of this genus encode the limiting enzyme for the synthesis of secondary bile acids, highlighting the fact that the appendix microbiome has an enrichment of the microbiota that metabolizes bile acids.

Dysregulated metabolic pathways

After the study, the bacterial species responsible for the production of secondary bile acids in the large intestine were elevated in the appendix. Thus, based on alterations in the microbiome, the researchers sought to see if Parkinson’s disease was associated with changes in microbial metabolic pathways In the Appendix.

The most significant change was a impaired lipid metabolism and a loss of fatty acid metabolism. Due to this dysregulated lipid metabolism, the team also tested whether proteins involved in metabolic pathways were also altered in the appendix and ileum.

Thus, in the appendix and ileum of people with Parkinson’s, there was a decrease in proteins that affect lipid metabolism. In addition, there was deterioration in the pathways involved in other cellular activity, in protein localization, antigen presentation, glycolysis, and immune activity.

Increased bile acids

The researchers also found changes in the microbiota involved in bile acid production when looking at the appendix. Bile acids are created in the liver, but act in the small intestine to break down fat and absorb important nutrients for the body. The liver synthesizes bile acids first from cholesterol.

The team studied 15 bile acids in samples from 15 people with Parkinson’s and 12 bile acids from controls. Compared to healthy controls, appendages from people with the condition had significantly increased bile acids secondarys, generally created for gut microbes.

The results showed an increase of 18.7-fold increase in lithocholic acid and a 5.6-fold increase in deoxycholic acid. Both compounds are toxic to cells in high concentrations.

On the other hand, there was no difference in the concentration of primary bile acids or total bile in the Parkinson’s appendix samples. There were also no changes in the concentration of primary bile acids in ileus. However, there was a 3.6-fold increase in lithocholic acid and deoxycholic acid.

Genetic changes

The next step was to see if Parkinson’s disease also genetically affected bile acid production. In the ileum of people with the condition, they found higher levels of gene transcripts which normally regulate bile acid and cholesterol homeostasis.

The authors suggest that Parkinson’s disease could alter bile acid control, regulate cholesterol levels, and overall fat metabolism.

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