A few weeks ago (Issue #534) I wrote about the role infections play in Alzheimer’s disease. Much of the focus of that article was on herpes viruses.
The herpes-dementia link is an important enough discovery to visit again, and go into in greater depth.
For one thing, it may finally move the pharmaceutical companies to shift their focus (so far unsuccessful) from amyloid-beta plaques in the brain to a completely different avenue of research that may hold real promise for treating Alzheimer’s.
Now that four new studies clearly demonstrate the herpes link, surely Alzheimer’s researchers cannot go on ignoring this important line of inquiry.
First Large-Scale Evidence for a Causal Link
It’s been tough going for molecular virologist Ruth Itzhaki.
Almost 30 years ago, she and her research group at the University of Manchester, England, found herpes simplex (HSV1) — the virus responsible for cold sores — in the brains of elderly people. Then in 1997, it was found to be a strong risk factor for Alzheimer’s.
Although 100 papers have been published by Prof. Itzhaki and other groups since, most scientists in dementia research remain uninterested in any link to infection.
As Prof. Itzhaki puts it, “Hostility or derision occurred with most of my papers on the topic, and many people simply ignored them.”
But a few months ago, she and her colleague Dr. Richard Lathe wrote a commentary in the Journal of Alzheimer’s Disease bringing attention to three new studies conducted in senior Taiwanese populations.
They highlighted the fact that these studies “provide the first population evidence for a causal link between herpes virus infection and senile dementia.”1
Antivirals Reduce Risk by 90%
The first study compared 846 older patients with herpes zoster ophthalmicus (shingles affecting the eyes) with 2,538 controls. After five years, 4.61% of the patients with the viral flare-up received a diagnosis of dementia, compared to only 1.65% of those without shingles.2
In the second study, each of 39,205 people with herpes zoster were matched by gender, age, and residence with the same number without the condition. They were followed up six years later.
After factoring in alcohol use and a number of different medical conditions, the shingles group had an 11% increased risk of dementia. But among sufferers prescribed anti-viral medication, the risk was reduced by 45%.3
The findings in the third study are even more extraordinary. 8,362 people over 50 with severe HSV1 were matched by gender and age to 25,086 subjects free of cold sores.
A decade later, the people in the herpes group were more than 2½ times more likely to develop dementia. Here again, those who were treated aggressively with antiviral medication saw the incidence of dementia reduced — this time by more than ten-fold.4
Commenting on these papers, Prof. Itzhaki believes “we are the first to realize the implications of these striking data on this devastating condition.”
Professor Lathe added, “Not only is the magnitude of the antiviral effect remarkable, but also the fact that…in most patients severely affected by HSV1 it appeared to prevent long-term damage in [the] brain that results in Alzheimer’s.”5
“The Most Compelling Evidence Ever Presented”
Another important study published this year adds to the weight of evidence supporting the role of a microbial infection in causing dementia.
The researchers analyzed post-mortem brain samples of those with and without Alzheimer’s, combined with advanced computer modeling that drew on a wide range of biological and genetic data.
The scientists found several types of herpes virus were much more abundant in the dementia group compared to the control samples. Some of the viruses also interacted with genes known to be involved with the development of Alzheimer’s.
One of the co-authors, Sam Gandy, professor of neurology at Icahn School of Medicine, Mount Sinai, New York, described their findings as “the most compelling evidence ever presented that points to a viral contribution to the cause or progression of Alzheimer’s.”6
How Infections Cause Dementia
Almost all of us have latent herpes viruses residing dormant within us. The problem comes when they’re woken up in the brain by infection, inflammation, a stressful event or a weakened immune system.
Lab research suggests that as the virus multiplies, amyloid beta protein is actually activated by the immune system to prevent viral replication. But if this process continues and the protein builds up to form plaques, it becomes problematic in itself — a type of friendly-fire which damages the tissues it’s trying to help.
This publication and the many doctors we’ve interviewed have long argued that the plaques are a reaction to inflammation or another disease process. They’re a symptom of some underlying cause.
While none of the studies can yet prove that infectious agents are the underlying cause of dementia, Chris Carter, a neuroscientist in the UK, believes that “viruses – and pathogens in general – must now be seriously considered as causal agents in Alzheimer’s.”
Ruth Itzhaki believes antiviral drugs “may have a strong part to play” in combating Alzheimer’s.
Is the scientific community listening?