Can you get Alzheimer’s disease from a gum infection? While the link may seem far-fetched, a new study has uncovered this lesser-known connection, offering clues to the roots of the neurodegenerative disease.
A number of scientific studies have demonstrated how Alzheimer’s could stem from an infection.
Growing research supports the viral infectious hypothesis of sporadic Alzheimer’s disease. Studies link several viruses — including herpes viruses (HHV-1 to HHV-7), flaviviruses (Zika, Dengue, Japanese encephalitis), HIV, hepatitis viruses (HAV to HEV), SARS-CoV-2, Ljungan virus, Influenza A, and Borna disease virus — to an increased risk of AD, mentions Ageing Research Reviews journal.
While one may not suspect an ordinary gum disease to turn into something incurable like Alzheimer’s disease, a study published in 2019 in Science Advances, indicates that it could root from a bacterial gum infection.
A team of researchers led by senior author Jan Potempa, a microbiologist from the University of Louisville, reported the discovery of Porphyromonas gingivalis – the pathogen behind chronic periodontitis in the brains of deceased Alzheimer’s patients.
This was also proved by a separate mice experiment where infection with the pathogen led to brain colonization by the bacteria. It also led to increased production of amyloid beta (Aβ), a protein that forms plaques in the brain and is associated with Alzheimer’s.
“Infectious agents have been implicated in the development and progression of Alzheimer’s disease before, but the evidence of causation hasn’t been convincing,” said the first author Stephen Dominy.
“Now, for the first time, we have solid evidence connecting the intracellular, Gram-negative pathogen, P. gingivalis, and Alzheimer’s pathogenesis.”
The bacteria also secreted toxic enzymes gingipains in the brains of Alzheimer’s patients, which correlated with – the tau protein, and a protein tag called ubiquitin, other markers for the disease.
The researchers also detected toxic gingipains in the brains of deceased individuals who had never been diagnosed with Alzheimer’s.
This finding is significant because, while P. gingivalis has been linked to the disease before, it remains unclear whether gum disease contributes to Alzheimer’s or if dementia leads to poor oral hygiene.
It also suggests that people with low levels of gingipains but not diagnosed with Alzheimer’s yet could have developed the condition had they 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 said.
There could also be a potential cure for Alzheimer’s keeping in mind this discovery as a compound formulated by the company called COR388, demonstrated in experiments with mice that it could cut bacterial load of a P. gingivalis brain infection, and also reduce amyloid-beta production and neuroinflammation.
“Drugs targeting the bacteria’s toxic proteins have so far only shown benefit in mice, yet with no new dementia treatments in over 15 years it’s important that we test as many approaches as possible to tackle diseases like Alzheimer’s,” chief scientific officer David Reynolds from Alzheimer’s Research commented in a statement.
Alzheimer’s disease and infections
Neuroscientist Rudolph Tanzi, director of the McCance Center for Brain Health at Harvard-affiliated Massachusetts General Hospital explained how infection might play a role in igniting amyloid-beta deposits and tau tangle.
“My colleague, the late Rob Moir, and I found that amyloid-beta is deposited in the brain in response to infection. It is a protein that defends against infection: it forms a web that entraps invading microbes,” Tanzi says. “In other words, amyloid-beta helps protect our brain from infection. That’s the good news. The bad news is that amyloid-beta also damages neurons which, over 10 to 30 years, starts to have obvious effects on cognition, ultimately leading to dementia.”
The chronic low-grade deposition of amyloid-beta leads to tau tangles that also destroys neurons and increases neuroinflammation, which could lead to further neuron death, setting off a cycle of neuron damage.
Dr. Anthony Komaroff, editor in chief of the Harvard Health Letter and professor at Harvard Medical School, says there is no single Alzheimer’s germ, but different microbes can play a role in triggering the disease.
