Parkinson’s Disease Medication and Bacteria in the Small Intestine

Study shows how gut bacteria affect the treatment of Parkinson’s disease

Source: News Medical Life Sciences

Jan. 18, 2019


Summary: Levodopa is a commonly used medication for people with Parkinson’s disease. This study was done to look into whether gut bacteria could be what’s contributing to the high variation in levels of levodopa that reach the brain in different patients. Levodopa is typically absorbed in the small intestine and can commonly be converted to dopamine and sent to the brain. The study found that the bacteria tyrosine decarboxylase present in the small intestines of rats did result in lower concentrations of the drug in the body, meaning the amount of bacteria present in the gut determines how effective the medication can be.


Connection:I would say this connects somewhat to what we have discussed in class because we have discussed anaerobic microbial cultures in areas such as animal guts. We’ve discussed how bacteria can have profound effects on people’s bodies. The abundance of this bacteria in the small intestine can affect many aspects of a person’s life when living with Parkinson’s disease. Examining the presence of bacteria and how they can alter other systems is something we have talked about briefly in class.


Critical Analysis: Admittedly, I think this article was fairly inconcise and indescriptive. However, I really thought the subject was interesting. I’d never thought about the gut to brain connections before, and the fact that it could affect the dosage results of medications so much is a little surprising to me. I wish the article would have included more on the nature of their methods and procedures as well. One thing I liked about how the article was written was the use of common language and phrasing which made it relatively easy to read and understand. This is an article I could see being read by most of the general public quite easily.


Question: I was a little confused on what happened to the Levodopa that was converted to dopamine. Would the increase in dopamine create side effects? And if so, what would they be and would they be of concern if the medication was to be significantly increased in order to increase Levodopa concentrations in the body?

A2 Microbes in the News (P.gingivalis and Alzheimer’s disease)

Article and Link:

“We may finally know what causes Alzheimer’s–and how to stop it’
By: Debora MacKenzie
Date: 24 January 2019


Researchers have found that the formation of amyloid and tau proteins which are signs of Alzheimer’s disease, may be a response to bacterial infiltration. One of the major risk factors of Alzheimer’s is the occurrence of gum disease caused by the bacteria Porphyromonas gingivalis.
They have found that P. gingivalis has been found to infect areas of the brain with Alzheimer’s lesions as well as exacerbating the symptoms of Alzheimer’s in mice who have been infected with P. gingivalis as gum disease. Similarly healthy mice (who have not been engineered to have Alzheimer’s) who have been infected with gum disease and the bacteria P. gingivalis, exhibit amyloid plaques, and neural damage similar to that found in Alzheimer’s affected brains.
Enzymes which P. gingivalis uses to feed on human tissue, have been found in 96% of brains analyzed by Cortexyme and P. gingivalis proper has been found in several brains upon autopsy. Higher rate of these “feeding enzymes’ called gingipains have been higher in those with a greater cognitive decline before their death as well as greater amyloid and tau accumulations.
Cortexyme has developed a molecule with inhibits these gingipains and has shown to effectively halt P. gingivalis infection in mice including stopping amyloid production and reducing the associated brain inflammation.


                      I can see a connection with the research that they are doing with Koch’s postulates. Not only have they found the pathogen in unhealthy mice, but also upon injecting the pathogen into healthy mice, they receive the same symptoms. I don’t know their exact procedure, however that they are not only exploring what they are finding within the diseased subjects, but duplicating the symptoms in healthy subjects is similar to how they have been identifying pathogens using these postulates.

Critical Analysis

I am very interested in this news story, not only because the community is expanding their thinking on the amyloid and tau protein buildup (previously thought to build up due to cell component aging) being a response to something, rather than an inevitable state of neural tissue. I also like that it goes into light detail on the reasoning behind why they began the studies, what the studies are doing and what the future of the studies are going to be. Also, it is interesting that they have not only made this correlation, but that Cortexyme has already begun developing a vaccine and medications to stop the proliferation of P. gingivalis in the brain (which could also help with gum disease, but I really just love the brains).
As for the article, I think that it is a lot of information for one article but that it is very well put together in a manner that doesn’t overwhelm the reader. There are also links embedded within the article that reference journal articles for further reading, which is beneficial for those who would like a deeper understanding.


The main question that I have is one of correlation vs. causation. There is evidence form the research on healthy mice that the P. gingivalis causes the anomalies within the brain tissue, but they did not find evidence of the bacterium in all cases of Alzheimer’s that they studied. So my question is still the age old question: Is this THE cause of Alzheimer’s disease or is it A cause of Alzheimer’s disease? Does it simply exacerbate the disease or increase the rate at which the disease presents?


Samantha Smith