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.
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?
1 Comment for “A2 Microbes in the News (P.gingivalis and Alzheimer’s disease)”
I found your article very enlightening. To be honest, Alzheimer’s disease has never affected me, nor anybody close to me, so I had never looked into how it worked other than what was covered in classes. I am very surprised that with all of this research, only now are we realizing that people have been looking into the wrong problem this whole time. I don’t know how to answer your question, as I have the same question. Although, now that they have this information I am guessing that the right answer might not be far away.