Gum Disease and Alzheimer’s

While there is some value to the current work, which extends our understanding of the link between gum disease and this form of dementia, we have to understand that the connections are likely very complicated, and the solution is probably more involved than just a single drug.

Gum disease is a chronic infection of the mouth. Many different species of oral bacteria colonize the area between the teeth and gums.

Like bacteria that cling to the teeth, these bacteria can release acid and other damaging chemicals to destroy the teeth, gums, and bone. This creates additional living spaces for the bacteria, first periodontal pockets, and later large areas of detached gums. Detached gums can begin to recede from the teeth.

As the number of bacteria around the teeth increases, the body responds. But the body’s response can be the worst part about gum disease. The immune system can attack and destroy the bone around your teeth, leading to loose teeth and even tooth loss. We’re not sure how much of this damage is due to the body exercising a kind of “nuclear option” trying to destroy bacteria along with gums and how much is due to oral bacterial corrupting the immune system.

The bacteria that cause gum disease can travel through the body via your blood vessels, potentially triggering similarly destructive immune responses elsewhere in the body.

Alzheimer’s disease is a degenerative brain disorder, and the leading cause of dementia among older adults in America.

The symptoms of Alzheimer’s disease can be mild at first. People have more difficulty remembering recent events than they do remembering details from their childhood. Eventually, people’s memory becomes so badly damaged that they can’t carry on conversations or perform normal everyday tasks.

Physical changes in the brain that correspond to the memory symptoms include the development of plaques and tangles in the brain. Plaques are buildups of a protein called beta-amyloid, Tangles are buildups of the protein tau. These buildups occur in the brain as part of normal aging, but for people with Alzheimer’s disease, the buildup happens more quickly, and follows a predictable sequence, starting with certain memory regions, then expanding out to more of the brain. Protein buildup in the brain has been linked to many potential causes, including sleep apnea, a sleep disorder in which a person wakes up many times a night. There is currently no cure for Alzheimer’s disease. However, treatment may slow the progression of the disease.

Alzheimer’s disease is the sixth leading cause of death in the US.

The current research is not the first time we’ve seen hints that gum disease and Alzheimer’s disease are linked. Investigation of the link began around 2000, when people started to suspect that systemic inflammation might play a role in Alzheimer’s development.

Systemic inflammation occurs when the body is plagued by chronic infection or other factors that trigger an ongoing immune response. The immune response transitions from a local counter to infection into a system-wide response, with potentially negative effects throughout the body. This research highlighted the role of many potential bacteria.

One common chronic infection is gum disease, which affects about half of all US adults, and two-thirds of adults over 65. As people began to look at the links between gum disease and Alzheimer’s, they found a surprisingly powerful connection.

Many studies started looking at the potential role of gum disease in triggering Alzheimer’s finding biochemical links between inflammatory markers and the brain damage leading to progressing dementia.

In 2017, a large population study showed that having gum disease for ten years or more was linked to a 70% higher risk of developing Alzheimer’s disease.

The current study looks at the role of one particular oral bacterium in the development of Alzheimer’s disease. Prophyroma gingivalis is a common bacterium in gum disease. Interest zeroed in on P. gingivalisafter a 2013 study showed that it was present in 40% of brains from a sample of Alzheimer’s disease victims, and in no brains of people without Alzheimer’s.

Then in October 2018, researchers published the results of a study showing that if healthy mice were exposed to P. gingivalis and its toxic byproduct, called gingipain, in the mouth for 22 weeks, they began developing brain damage effects that were similar to Alzheimer’s disease. This included damage to the hippocampus, a key memory structure, and buildup of amyloid beta, which likely has an antibacterial role.

The new study expands on this finding, although it is an unconnected study performed by a different research team. This team took brain core samples from postmortem brain samples of people with Alzheimer’s disease and those without. They found that Alzheimer’s disease diagnosis and symptoms correlated with the level of toxic byproducts from oral bacteria found in the brain.

Researchers then performed a similar infection study with mice. They gave mice P. gingivalis orally, and were able to show that the bacteria moved to the brain, leading to the buildup of amyloid beta. Then researchers tried the infection step again, only this time they applied an inhibitor that targeted key gingipains P. gingivalis relies on to spread through the body. This prevented the spread of the bacteria to the brain, and, therefore, stopped the buildup of amyloid beta.