St. Lawrence Dentistry is fortunate to have many senior patients and we strive to do our small part in helping them maintain and elevate their health. With advanced age comes some challenges and Alzheimer’s disease has been most definitely one of them. Research keeps evolving and a landmark study suggests mouth bacteria may be linked to Alzheimer’s disease.
After years of frustration there are new leads on the research of Alzheimer’s disease. Interesting correlations have emerged which suggest that the ailment is caused by a bacteria highly involved in gum disease. This could prove to be of pivotal importance in developing treatments for this enigmatic condition.
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In the past dementia was not as common since people did not live as long. Now it is the fifth biggest cause of mortality. Alzheimer’s makes up more than two-thirds of dementia cases. This unfortunate malady is characterized by declining memory and thinking ability over a decade or so. Many of us can relate as we have had family members who have been afflicted which this shattering condition. It is no short of devastating to both those who have it and their loved ones.
This affliction is often characterized by the gradual gathering of 2 types of proteins—called amyloid and tau— in the brain. These form overarching sticky plaques in the brain’s vital centres. However, some people in their late eighties and beyond have brain plaques without having cognitive issues. This has recently led researchers to debate whether amyloids have a distinctive role in Alzheimer’s disease.
In 2016 investigators reasoned that the role of amyloid seemed to be a sticky protective layer against bacteria. They found that the protein can function as an anti-microbial compound that neutralizes bacteria. At that time it was believed that the amyloid in it of itself went on to give rise to the brain damage of Alzheimers, not bacteria. However, the general opinion on this seems to be transforming with subsequent analysis. Bacteria have been located in the brains of individuals with Alzheimers. However, it has not been clear whether the bacteria caused the disease or they were simply able to gain access to the brain impaired by Alzheimers.
Porphyromonas gingivalis is the main bacteria found in gum disease and is a known risk factor for Alzheimer’s. So far researchers have found that P.gingivalis spreads into and inflames brain regions affected by Alzheimer’s disease.
Investigators found two harmful enzymes P.Gingivalis uses to feed on human tissue in over 95% of brain samples taken from the hippocampus part of the brain— the region critical to memory. Furthermore, genetic material from P.gingivalis was also found in the cerebral cortex of the brain which is critical for conceptual thinking. It is now postulated that P.gingivalis not only enters the brain as a result of Alzheimers, but also could be a part of the disease genesis.
Experiments involving mice have also shed light on this subject. Research teams infected mice with gum disease and this lead to brain infection, amyloid production, tangles of tau protein, and neuron damage. This seems to demonstrate causation.
It is unknown exactly how P.gingivalis accesses the brain. There are feasible courses it could take. When plaque forms at the edge of your teeth it causes ‘periodontal pockets’ in which P.gingivalis can flourish and secrete toxins. This inflammation can culminate in bone and tooth loss. In fact some investigations have demonstrated that people with less teeth have an increased probability for dementia. The inflammation and toxins secreted by P.gingivalis degenerate the lining of your mouth which makes it easier for bacteria to infiltrate the blood stream and invade other organs.
In health, the blood-brain barrier helps shield against microbes. However, P.gingivalis can diffuse into white blood cells and may enter the brain in that manner. They also may attack cranial nerves near the mouth, then metastasize from cell to cell toward the brain over a period of years.
There are 2 main ideas on how P.Gingivalis may cause dementia. It may prompt the release of amyloid. The amyloid may incase the bacteria in an attempt contain the infection. The incasement may also unfortunately suffocate and kill neurons. Another possibility is that P.gingivalis may directly damage the brain. It is widely recognized that Alzheimers involves inflammation in the brain which ends up annihilating neurons. P.gingivalis is known to cause inflammation of the gum tissue so it may do the same in the brain.
Other researchers have expressed reservations about a possible link of Alzheimers to gum disease saying that a persons genes are what onsets Alzheimers. However this bacterial postulation does not conflict with this as the combination of both genetic and bacterial status may mix together to determine a persons susceptibility to the disease. Some people have said the if the bacterial hypothesis is true then our ancestors should have had more incidences of dementia because oral hygiene was poorer in antiquity, However, in previous generations life expectancy was far less, hence people did not live to the advanced age at which Alzheimers is more common.
It’s too early to tell if this bacteria hypothesis will be confirmed with more research. However, considering what has been found so far it is prudent to do everything possible to prevent gum disease in yourself. Cleaning your teeth twice a day, flossing or using interdental sticks to remove plaque can be of great help in preventing gum disease. It is important not to brush too hard as this may usher bacteria to enter your blood stream. If plaque accumulates it can turn into hard calculus which encourages the growth of more plaque. This cannot be removed by regular brushing. Fortunately, a dental hygienist can easily remove this unwanted calculus.
To learn more about dental cleanings at St. Lawrence Dentistry please visit us here.
We hope you have found this article informative. Please give is a call if you live in the Mississauga area would like to further investigate how your oral health may affect your total health.
Reference: New Scientist Feb/2019