Does gum disease cause Alzheimer’s disease?

Alzheimer's disease linked to gum disease

Does gum disease cause Alzheimer’s disease? A new research article explains how periodontal (gum) disease bacteria is linked to the terrible mental condition.

A growing number of scientific studies have given credence to the theory that Alzheimer’s disease (AD) is an infectious process. While the exact mechanisms of this infection are something researchers are still trying to determine, many scientific papers argue the deadly spread of AD goes way beyond what we used to think.

In a new paper led by senior author Jan Potempa, a microbiologist from the University of Louisville, researchers report the discovery of Porphyromonas gingivalis (P. gingivalis) – the pathogen behind gum disease – in the brains of deceased AD patients.

It’s not the first time gum disease and AD have been linked, but in this new article published in Science Advances magazine, the researchers went further.

In separate experiments with mice, oral infection with the pathogen led to brain colonization by the bacteria, together with increased production of amyloid beta (Aβ), the sticky proteins commonly associated with AD.

The research team, which is coordinated by pharmaceutical startup Cortexyme that was co-founded by first author Stephen Dominy, isn’t claiming to have discovered definitive evidence of Alzheimer’s causation just yet. But it’s clear they think there is a strong line of investigation here.

In addition, the team identified toxic enzymes called gingipains secreted by the bacteria in the brains of AD patients, which correlated with two separate markers of the disease: the tau protein, and a protein tag called ubiquitin. But even more compellingly, the team identified these toxic gingipains in the brains of deceased people who were never diagnosed with AD.

That’s important, because while P. gingivalis and the disease have been linked before, it’s never been known whether gum disease causes AD, or whether dementia leads to poor oral care. The fact that low levels of gingipains were evident even in people who were never diagnosed with AD suggest they might have developed the condition if they had lived longer.

“Our identification of gingipain antigens in the brains of individuals with AD and also with AD pathology but no diagnosis of dementia argues that brain infection with P. gingivalis is not a result of poor dental care following the onset of dementia or a consequence of late-stage disease, but is an early event that can explain the pathology found in middle-aged individuals before cognitive decline,” the authors write in their paper.

So what can this mean in terms of dental care? If chemicals created by one of the main bacteria responsible for gum disease is found in the brain of people with AD and AD symptoms, it stands to reason that keeping your teeth and gums clean may reduce your risk of developing AD. This includes consistent home care (brushing and flossing daily), maintaining regular dental checkups with a dentist, and if gum disease is present, having it treated with deep cleaning and/or and advised surgical treatment. If further research can confirm causation of Alzheimer’s disease from periodontal disease, this will be a very exciting development in dentistry, as diligent oral health care could help prevent a disease that is very troubling to many people throughout the world.

At AdVance Dental’s blog page we also have info about the link between periodontal disease and stroke and diabetes. Read about how some foods can make it harder for bacteria to colonize on teeth here.

Check out our YouTube Channel for educational videos about our practice, dentistry, and more!

References:

https://www.sciencealert.com/new-evidence-reveals-an-unexpected-culprit-behind-alzheimer-s-disease?fbclid=IwAR1LG-6g0Wlua9iJsq4roKjDRW5wSGfbzKkkel3m5YtcoNyGVImJK1H88ms

Dominy S. et al, Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors, Science Advances 23 Jan 2019: Vol. 5, no. 1, eaau3333, DOI: 10.1126/sciadv.aau3333

 

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