Gum infection could be linked to Alzheimer’s, study says

Blood test could detect Alzheimer’s up to 16 years before symptoms begin, study says

Blood test could detect Alzheimer’s up to 16 years before symptoms begin, study says

In October 2018, Cortexyme announced results from its Phase 1b clinical trial of COR388 at the 11th Clinical Trials in Alzheimer's Disease Conference.

It showed that the bacterium Porphyromonas gingivalis-which is the pathogen famous for causing chronic gum disease-is found in the brains of Alzheimer's disease patients.

"Now, for the first time, we have solid evidence connecting the intracellular, Gram-negative pathogen, P. gingivalis, and Alzheimer's pathogenesis".

While the exact mechanisms of this infection are something researchers are still trying to isolate, a litany of papers argue the deadly spread of Alzheimer's goes way beyond what we used to think.

An enzyme called gingipains, which the Porphyromonas gingivalis (P. gingivalis) bacteria gives off, is the "main cause of Alzheimer's disease", Dr. Steve Dominy, study author and associate professor at University of California, told Newsweek.

"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 effect 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. Alzheimer's disease is the fastest growing epidemic in America. Dominy began a side project looking for P. gingivalis in brain tissue from deceased patients with Alzheimer's, and-after his work found hints-started the company with entrepreneur Casey Lynch, who had studied Alzheimer's as a graduate student. They found toxins called gingipains produced by P. gingivalis in 96% of the samples and the bacterium itself in three samples.

Almost six years ago, Lynch received a call from Stephen Dominy, a psychiatrist at the University of California, San Francisco, who had studied the link between HIV and dementia.

Still, Edelmayer says with so much still unknown about the disease, studies like this are important for gaining a better understanding of Alzheimer's. 'A couple of years ago it was suggested [amyloid] accumulation might actually be part of the brain's innate immune system for dealing with bacteria, ' he says. "What this paper shows is their pre-clinical data - or at least the parts of it they want to show the world - that helps to strengthen their story, ' he says".

"Not enough people are asking what is upstream of the plaques ... and [brain] inflammation", said Lynch, who has a background in Alzheimer's research and was frustrated by the string of failed therapies for the disease. Dominy agrees. 'Certainly, reducing the P. gingivalis load in the mouth, especially at an early age, should be taken more seriously than it now is based on our data, ' he says, though he adds that merely targeting gum disease is unlikely to help with infections of P. gingivalis in the brain.

There is hope that the blood test will eventually be useful for a wider range of people who may be at risk of the common form of older-onset Alzheimer's disease known as "sporadic", as well as those with the genetic version.

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Image copyright Getty Images What do other scientists say about the study?

The mice also showed a build-up of beta amyloid, one of the damaging proteins in the brain thought to cause dementia.

'Everyone's life can be improved by regular appointments and good oral hygiene, reducing the bacterial load that's ever present in our mouths to a level that's unlikely to cause tooth decay, gum disease or tooth loss'.

This disrupts the transmitters that carry messages, and causes the brain to shrink.

However, he said the study was limited because the team has not yet determined if different strains of P. gingivalis are more virulent than others in causing brain infection.

More than 5 million people suffer from the disease in the U.S., where it is the 6th leading cause of death.

As brain cells die, the functions they provide are lost.

The progress of the disease is slow and gradual.

The patients carrying the gene mutations predisposing them to Alzheimer's disease - a group of 243 - were found to have increasing levels of NfL compared to the control group, consisting of 162 family members without the mutation.

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