As early as 2017, Japanese researchers from Kyushu University in Fukuoka discovered in a study a connection between bad teeth and Alzheimer’s. They collected data from around 1,600 volunteers aged 60 and over and found that oral hygiene had a direct influence on mental health: the fewer of their own teeth older people still had, along with how poorer the condition that their teeth were in, the higher their risk of dementia or Alzheimer’s disease became.
The results of the study show that the likelihood of dementia rose by 60 to 80 percent in people with 20 or fewer teeth. To be precise, the probability of developing dementia was 81 percent for people who had 1 to 9 teeth left. For people with 10 to 19 teeth, the figure was 63 percent. At the same time, the fewer teeth the test subjects had, the greater the risk they had of developing Alzheimer’s.
The Japanese researchers’ theory that bacterial infections such as periodontitis – along with a genetic predisposition – could be responsible for the development of dementia, has now been corroborated by research from Norwegian scientists. In a study published in the scientific journal Science Advances, they found that germs which cause periodontitis are able to enter the brain. There they can cause Alzheimer’s disease through toxic enzymes.
Periodontitis bacteria migrate into the brain
The study focused on the microbe porphyromonas gingivalis which causes periodontitis and other inflammations in the mouth. As people who suffer from severe forms of periodontitis also suffer from Alzheimer’s disease more frequently, the researchers suspected a connection. They believed that the bacteria caused damage not only in the oral cavity but also in the human brain.
The mouse-based model has already shown that pathogens can enter the brain through the mouth, where they then trigger infections. Scientists from a pharmaceutical company have also found more DNA of the Porphyromonas gingivalis bacteria in the brain tissue of deceased Alzheimer patients, than they found in deceased people who did not have Alzheimer’s disease. Furthermore, according to the results of the study, the toxic enzyme gingipain was found in 51 of 53 brains of the deceased Alzheimer patients examined. It was also found that the more the brain was affected by Alzheimer’s disease, the higher the stress on the brain. Consequently, there seems to be a correlation between the development and progression of Alzheimer’s disease and the oral bacterium, the researchers explained.
The mice also showed that gingipain trigger inflammations in the brain and thereby cause an increased production of the protein beta-amyloid. This protein is a substance that is typically found as a deposit in the brain of Alzheimer patients. The enzyme was also responsible for damage to tau proteins in the brain. They are of critical importance to neurons and are often malformed in Alzheimer patients.
Effective inhibitor against gingipain
As part of the study, the scientists also investigated ways of preventing the effect of gingipain in the brain. They found an inhibitor consisting of a molecule that is able to pass through the blood-brain barrier. It was able to block the effect of the enzyme in the brain of mice infected with the Porphyromonas gingivalis bacteria. In these animals, a significant reduction in stress on the brain was observed as soon as the inhibitor was administered orally. Protein deposits in the brain also decreased significantly, resulting in fewer neurons being damaged.
Following the successful tests with mice, clinical trials with human volunteers have already begun. The researchers hope that “the inhibitor could slow down or even stop further neurological degeneration in Alzheimer patients”.
To prevent dementia or Alzheimer’s disease, the researchers recommend: “brushing your teeth regularly and using dental floss”. In this way, it can be prevented that periodontitis pathogens develop in great numbers and reach the brain. However, the scientists also emphasize that Alzheimer’s is not caused exclusively by periodontitis pathogens.
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