Floss Your Teeth!

The health of your teeth and gums has long been known to affect a number of aspects of heath, and even fatal consequences can emerge from gum infections.  We all hate it, but we're encouraged to floss our teeth every day!

So what about Alzheimer's disease?  Can gum disease promote, or even cause AD?  Can gum disease be a complete explanation for AD??  This thought has been around for a while now, but it's finding new energy.  (Prompted by Dale Bredesen's research at UCLA, we bought a Water Pic, which is said to do a better job with gum health than conventional floss.)

On January 23, 2019, NewScientist magazine published a story on a possible relationship between gum disease and AD.  The article immediately began trending on the internet, and several friends and family sent me links about it (all appreciated).

While the article acknowledged that the relationship wasn't proven, it seemed to characterize the link as almost certain and possibly the whole story of AD etiology.  That someone was seriously considering that it might be the whole story on AD sure caught me by surprise. 

According to the article, the culprit is the bacterium P. gingivalis which is able to enter the brain in a way that bypasses the blood-brain barrier.  P. gingivalis has been found in the brains of people with AD, and it appears to be associated with the generation of beta amyloid proteins, one of the hallmarks of AD.  The function of beta amyloid has been debated for a long time, and many believe it results from a misguided cutting of a precursor protein.  The function of the precursor protein is also unknown.  Some believe the amyloid is a central feature of the destruction of brain cells in AD, while others believe it's an innocuous byproduct of the disease process.  Certainly, the amyloid hypothesis has come under serious scrutiny in the past year or so, as drugs that removed amyloid plaques failed to improve cognition.  The article quotes researchers who speculate that amyloids may exist simply to neutralize P. gingivalis.

A tantalizing idea is that it may be possible to develop a vaccine against P. gingivalis, and therefore against AD.  Wouldn't that be great?

The idea of a vaccine against AD is not new.  Here is an example of a lawyer, her Hawaii real estate developer husband, and her researcher mother who may be having success with a vaccine.  It's a family project.  However, it does not focus on P. gingivalis, and its theory seems to be rooted in the amyloid hypothesis.  We'll see how the trials work out, but early results seem to have been positive.

In considering the possible role of P. gingivalis in AD, the question arises regarding the obvious role of genetics.  In the case of younger onset version of AD the disease is entirely a consequence of genetics.  For the "sporadic" (common) version of AD the gene that codes for the ApoE4 variant of the ApoE protein certainly increases the probability of developing AD.  So how can you claim that infection by this bacterium is entirely responsible for AD, when we know that genetics plays such an important role?

There is an explanation.  A laboratory found that P. gingivalis breaks up ApoE proteins into constituent amino acids.  The ApoE4 protein contains more of a particular amino acid that, when released, may harm nerves.

This is all fascinating, but I have to admit to a level of skepticism.  The story seems to pat.  But -- who knows?  With the steady erosion of the amyloid hypothesis, maybe this does explain it all.