If not amyloid, let's take another look at the herpes virus

One of the tragedies of the ongoing amyloid scandal is that pursuing the possibly flawed amyloid hypothesis for Alzheimer's disease may have distracted us from other pathways to effective treatments.  One of those pathways might be through the herpes virus and its suspected role in the development of the disease.  

Back in June 2018 and January 2020 we wrote about evidence that the herpes virus may be among several pathogens that spark the development of Alzheimer's disease.  Some studies found more herpes viruses in the brains of people dying of Alzheimer's disease, but this was not confirmed in other studies.  Nevertheless, there has been a longstanding association between herpes infections and the development of the disease, although how this occurs has not been clear.  But maybe there has been a breakthrough.

A recent study at Tufts University and the University of Oxford  developed an hypothesis about how this happens, and it involves two different versions of the herpes virus, herpes simplex (HSV-1) and varicella zoster (VCV).  HSV-1 is known to cause cold sores around the mouth, while VCV first causes chicken pox and later shingles.  Perhaps you're familiar with these.

As we noted in our earlier posts, after an infection, HSV-1 can take up residence in brain cells and remain innocuously dormant there for a long time.  Until VCV shows up. 

Both viruses attack nerve cells and cause inflammation.  If, like me, you've had shingles, you know that it produces a rash-like appearance of tiny red dots on your skin.  Those red dots are the inflamed ends of nerves reaching from the brain to the surface of the skin.  That's why shingles is so painful.  It also indicates that there is inflammation in the brain, and brain inflammation is an important factor in the development and progress of Alzheimer's disease.

What the researchers found was that an infection with VCV may somehow "activate" the HSV-1, causing it to promote inflammation and the development of the amyloid plaques and tau tangles that define Alzheimer's disease.  

But there may be ways of activating HSV-1 other than by VCV.  In Beating the Dementia Monster, we discussed an association between the development of Alzheimer's disease and factors like head trauma, alcohol consumption, and obesity.  The authors of the study suggested that these could promote the disease by activating the HSV-1 virus on their own, since HSV-1 is already resident in the brains of most of us.

So, how about stopping the VCV from activating HSV-1?  The authors of the study say you should get your shingles shot!  There is already an association established between people who get the shingles shot and a reduced risk of Alzheimer's disease, something I didn't know before reading this study.

I have wondered before why I developed Alzheimer's disease, when I don't have any of the commonly associated risk factors, such as the APOE4 gene.  Maybe this is the answer.  I had a serious case of shingles when I was in my early 30s, but I experienced two more episodes in the following decades.  To the best of my recollection, the most recent episode was about 15 years before my diagnosis in 2015.  As we discussed in Beating the Dementia Monster, the disease is thought to begin about 15 years before the appearance of the first symptoms.  So maybe that's the answer I've been looking for to my question, "Why me?"  

(I'm not whining when I say, "Why me?"  The years since my diagnosis have been some of the richest years of my life.)