What kicks off the process that leads to Alzheimer’s? Decades of research has failed to come up with an answer. One area that’s been largely ignored is the role played by viruses.

Mounting evidence points to HSV-1, the cold sore virus, as a prime suspect. But it doesn’t work alone. Let’s examine the recent science and see what it means to you and what you can do about it…

Solid scientific evidence implicates infectious agents in the development of Alzheimer’s disease, but funding for this area of research has been difficult to come by.

Scientists like to go where the research funds are headed. That’s where the action is, and for Alzheimer’ disease, that’s amyloid plaque research. And those researchers who investigate areas where there won’t be a financial or career payoff, don’t usually get much attention.

Take molecular virologist Ruth Itzhaki, who has been at the forefront of viral research, but, as she puts it, “Hostility or derision occurred with most of my papers on the topic, and many people simply ignored them.”

Despite these attitudes, Professor Itzhaki and her colleagues at the University of Oxford remain undaunted. Recently she teamed up with colleagues at Tufts University in Greater Boston to produce more groundbreaking research.

Cold Sore Virus Implicated

Prof. Itzhaki had previously focused her attention on the potential role of herpes simplex virus type 1 (HSV-1), the type that causes cold sores. It’s estimated that half the world’s population under the age of 50 has been infected with HSV-1. It usually lies dormant within nerve cells, but stress and a depressed immune system can reactivate it.

Since so many people are stressed out today and have less than optimal immune systems thanks to toxicity and poor diets, a potentially large number of people could be on the road to Alzheimer’s.

Over the last three decades Prof. Itzhaki’s lab has shown that HSV-1 DNA is present in the human brain in a high proportion of older people. What’s more, her team discovered that the virus, when in the brain – in combination with a specific genetic factor – confers a high risk of developing Alzheimer’s. And in addition, there are major links between the effects of the virus and the characteristic features of the disease.

Best of all, Prof. Itzhaki and her team have discovered that treating lab-grown HSV-1-infected cells with antivirals protects against Alzheimer’s.

Virus Triggers the Accumulation of Amyloid Plaque

Support also comes from Tufts. They showed that when the virus is activated, it leads to neuroinflammation, accumulation of amyloid beta and tau proteins, and loss of neuronal function – all signature features found in Alzheimer’s patients.

David Kaplan, Stern Family Professor of Engineering at Tufts, said, “We have been working off a lot of established evidence that HSV has been linked to increased risk of Alzheimer’s disease in patients.”

A One-Two Infectious Punch

In the latest study, published in the Journal of Alzheimer’s Disease in August, Prof. Itzhaki, Prof. Kaplan, and Dana Cairns, also from Tufts, researched varicella zoster virus (VZV), another type of herpes virus which causes chickenpox and shingles.

Using both lab-grown brain cells and a 3D bioengineered brain-like tissue model they found VZV infection didn’t cause amyloid clusters or tau tangles to form. But they did witness gliosis – a response to the infection in glial cells that leads to scarring – and up-regulation of inflammatory cytokines. What does this mean? Their findings suggest VZV harms the brain but is unlikely to be a direct cause of Alzheimer’s.

However, when they infected cells that contained latent HSV-1, the virus was reactivated, and the team saw a dramatic increase in levels of amyloid and tau. This suggests severe VZV infection in humans, as in shingles, could reactivate latent HSV-1 in the brain, which, in turn, could lead to the formation of Alzheimer’s-like damage.

Prof Itzhaki explained, saying, “This striking result appears to confirm that in humans, infections such as VZV can cause an increase in inflammation in the brain, which can reactivate dormant HSV-1.

“The damage in the brain by repeated infections over a lifetime would lead eventually to the development of Alzheimer’s dementia.”

Dana Cairns agrees. “It’s a one-two punch of two viruses that are very common and usually harmless, but the lab studies suggest that if a new exposure to VZV wakes up dormant HSV-1, they could cause trouble.”

What Can You Do?

There’s good news: The evidence suggests that antiviral drugs can prevent damage from these infectious agents. What’s more, the scientists encourage people over the age of 50 to get the shingles vaccine to prevent the infection from ever taking hold. And if you’ve had shingles, you’re still encouraged to get the vaccine, called Shingrix.

Shingrix is a non-living vaccine made up of a component of the virus. It’s given in two doses, spaced between two and six months apart.

  1. https://www.ox.ac.uk/news/2022-08-02-viral-role-alzheimers-disease-discovered
  2. https://engineering.tufts.edu/news-events/news/common-viruses-may-be-triggering-onset-alzheimers-