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The Relationship Between Alzheimer’s and Gum Disease

In a recent study, researchers have identified a link between Alzheimer’s disease and the bacteria present in gum disease. This study, conducted by researchers at the pharmaceutical company Cortexyme, sought to examine the role that Porphyromonas gingivalis (P. gingivalis) played in the development and progression of Alzheimer’s. P. gingivalis has previously been studied by other researchers and shown to be linked to heart and respiratory conditions. Evidence shows that the pathogen can migrate from the mouth to other organs and cause similar destructive and inflammatory damage.  

Cortexyme researchers found that P. gingivalis was present in the brains of patients with Alzheimer’s disease. Studies were also conducted using lab mice in which certain proteins associated with cognitive degeneration and P. gingivalis were identified. As a result of these findings, researchers believe that inhibiting proteins produced by P. gingivalis can be used as a treatment for Alzheimer’s. Read the sections below to learn more about these studies and findings and what they mean for Alzheimer’s research and treatment. 

What is Alzheimer’s disease? 

Alzheimer’s is a neurological disease that causes progressive deterioration in the brain. The resulting decline in cognitive ability leads to memory loss. Eventually, sufferer’s ability to perform certain basic activities is affected and he or she will need full-time support from others. 

Researchers and doctors are still unsure about the primary cause of Alzheimer’s. Numerous studies exist with the intent of discovering the source or sources of the disease. Current understanding indicates that brain cells are destroyed as the disease progresses. Brain cell death occurs as a result of built-up plaque and tangling of nerve cells. Proteins known as beta-amyloids are involved in plaque build-up. The tangling of brain cells is related to another protein called tau. 

Alternatively, Alzheimer’s is also theorized to be a result of genetic factors and/or chronic inflammation. While genetics are difficult to control, inflammation has numerous causes that can be avoided. For instance, infections and physical trauma can both causes inflammation. After a lifetime of repeated exposure to inflammation, the brain will be affected. The research study discussed in this article focuses on the buildup of amyloids in the brain as a result of infection. 

Although researchers know which proteins are involved in the progression of Alzheimer’s, they do not yet understand how or why the process begins. However, this recent study conducted at Cortexyme offers some insights. Specifically, the research sheds light on how beta-amyloid proteins accumulate in the brain.  

What is periodontal disease?

Periodontal (gum) disease is an inflammatory infection in the mouth that causes damage to the gums and surrounding tooth tissue. While there are hundreds of bacteria that contribute to the disease, Porphyromonas gingivalis is one of the major pathogens the affects gum tissue.

  1. gingivalis functions both directly and indirectly to progress the infection. This means that the pathogen itself, as well as the proteins it produces, contribute to the inflammatory response produced by the body. Moreover, the presence of harmful periodontal bacteria is associated with other health conditions besides gum disease including pulmonary disorders and heart diseases.

Research into these other conditions indicates that the bacteria is not isolated to gum tissue. Thus, it is able to spread to other organs and cause damage. Based on these findings, Cortexyme researchers hypothesized that P. gingivalis could affect the brain in similar ways. 

What they also discovered was that the pathogen produced gingipains which are toxic enzymes. In the deceased Alzheimer’s patients that were studied, larger amounts of gingipains were observed in those with more Alzheimer’s-related proteins. 

How P. Gingivalis Might Contribute to Alzheimer’s 

Previous studies involving P. gingivalis have indicated that the bacteria is able to move to the brain from the mouth. However, the most recent research shows DNA evidence of the bacteria’s effects in the brain. A key finding in the study is that P. gingivalis produces an enzyme that attacks and destroys nerve cells in the brain. 

In the study, researchers at Cortexyme found that in 96 percent of the 53 people with Alzheimer’s that they studied, an enzyme produced by P. gingivalis, called gingipains, was present. The significant fact about this enzyme is that it contributes to the destruction of neurons by attacking essential proteins.  

Another experiment conducted by the same team, P. gingivalis bacteria were observed in rats. The researchers gave healthy mice swaps of P. gingivalis for six weeks. Then, they found that the pathogen colonized in the brains of the rats. Additionally, the brains showed evidence of increased beta-amyloid production as well as gingipains presence. The gingipains affected the tau proteins, which are responsible for normal neuron function.

The results showed that the presence of gingipains was toxic to tau. Moreover, a protein called ubiquitin that is found on damaged proteins, tau tangles and beta-amyloid plaque were found in abundance. Thus, the presence of P. gingivalis was concluded to influence the buildup of plaque in the brain and neurodegeneration. 

Further experimentation tested molecular therapies that blocked the toxic proteins created by P. gingivalis. These inhibitors blocked the production of beta-amyloids and reduce inflammation in the brains of rats. The first phase of the clinical trials showed positive results. 

Elderly Alzheimer’s volunteers showed some signs of improvement. The mice that were tested for the therapy also demonstrated improved cognitive function. Because of these results, the research suggests that a gingipains inhibitor can be used as a treatment for Alzheimer’s.

Why Some Researches Do Not Agree

Even with the evidence pointing to the link between specific pathogens and cognitive decline, some researchers believe there is not sufficient evidence to verify this claim. This because the study conducted by the Cortexyme company was small-scale. Thus, many researchers need additional testing, samples and replication. 

Furthermore, while the research team did acquire some evidence from deceased Alzheimer’s patients, other components of the study were performed on mice. Although they found that P. gingivalis correlated with the accumulation of beta-amyloids, they cannot conclude that it caused the buildup. 

Thus, some researchers do not find that to be sufficient evidence for the claim that P. gingivalis and its associated proteins cause Alzheimer’s. While the data and results of the experiments do fall in line with the general consensus that Alzheimer’s is triggered by brain inflammation, it is not conclusive as to whether bacteria triggers the inflammation.