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Another study ties Alzheimer’s progression to bacteria in your mouth

A common type of oral bacteria associated with periodontal disease has been linked to neuroinflammation and the progression of Alzheimer’s disease. The research, from an international team of scientists, builds on a prior body of evidence linking poor oral health with dementia and neurodegeneration.



Researcher studying an xray
Researchers have found mice infected with a certain type of oral bacteria displayed faster progression of Alzheimer's symptoms compared to uninfected animals

The idea that gum disease plays a role in the onset or progression of Alzheimer’s disease is a hypothesis that sits on the fringes of dementia research. But over the last few years a growing number of scientists have begun to take the idea somewhat seriously, and studies have slowly started to dig into the association.


Most research so far has focused on the possible ways Porphyromonas gingivalis (Pg), the bacterium responsible for most gum disease, could influence the brain, either directly or indirectly. This new study turned its focus to another type of oral bacteria, Fusobacterium nucleatum, which is known to increase in volume in the presence of periodontitis.


Across a series of robust animal experiments the new research demonstrated how F. nucleatum can increase the proliferation of immune cells in the brain. This inflammatory response was then seen to accelerate the progression of Alzheimer’s in animals bred to model the disease.


"In this study, our lab is the first to find that Fusobacterium nucleatum can generate systemic inflammation and even infiltrate nervous system tissues and exacerbate the signs and symptoms of Alzheimer's disease," explained Jake Jinkun Chen, from Tufts University School of Dental Medicine.


The findings do not suggest this oral bacteria directly causes Alzheimer’s disease. Instead, the researchers say the bacteria, “accelerates the development of disease by promoting inflammatory responses in the brain, exacerbating the behavioral and pathological manifestations [of Alzheimer’s]."


Several questions still remain unanswered, particularly in regards to exactly how this bacterium causes the direct damage to brain tissue. The new study found no trace of F. nucleatum in brain tissue, which adds weight to the hypothesis that some kind of inflammatory response to the pathogen is crossing into the brain and influencing neurodegeneration.


The study points to two potential pro-inflammatory proteins activated by F. nucleatum that have previously been associated with neurodegeneration. This offers a plausible way by which the oral bacteria could be accelerating the progression of brain diseases such as Alzheimer’s. But it is still too early to suggest these findings will lead to a new therapeutic treatment for Alzheimer’s.


Ultimately, Chen said his team’s findings should be a sign for doctors to take notice of oral health in patients, particularly those facing the earliest stages of cognitive impairment. He believes it is possible effective treatment of periodontal disease could slow the progression of diseases such as Alzheimer’s.


“Our studies show that F. nucleatum can reduce the memory and thinking skills in mice through certain signal pathways,” Chen said. “This is a warning sign to researchers and clinicians alike. Testing for bacterial load and degree of symptoms could one day become a way to measure the effects of F. nucleatum and manage treatment to slow progression of both periodontal disease and Alzheimer’s.”


The new study was published in the journal Frontiers in Aging Neuroscience.



*Article published on New Atlas by Rich Haridy


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