We just got more evidence that two common viruses can team up to cause Alzheimer’s: ScienceAlert

An experiment on model brains has added more evidence to the hypothesis that the viruses responsible for chicken pox and herpes may combine to cause Alzheimer’s disease.

While the claim remains hotly debated, researchers at Tufts University and Oxford University say they have just demonstrated the presence of two viruses in tandem that can stimulate an excess of proteins responsible for Alzheimer’s characteristic brain plaques.

The potential link between herpes simplex virus (HSV-1) and Alzheimer’s disease has already attracted attention over the years. Not only has its DNA been found in large amounts in the brains of older people, those who have a gene linked to Alzheimer’s disease may have an increased risk of developing the disease if they also have HSV-1.

Like the herpes virus, the varicella-zoster virus can lie dormant in nerve cells for years, emerging later in life to wreak havoc like shingles.

It is possible that the resulting inflammation increases the risk of dementia, but shingles rarely flares up more than once or twice in a lifetime. It was thought to be barely enough to cause Alzheimer’s.

Yet there are good reasons to suspect that the two conditions are somehow related. Population-based studies in Taiwan, the UK, South Korea and the US suggest that vaccination against re-emergence of varicella-zoster virus such as herpes zoster reduces the risk of dementia, for example.

To get a better idea of ​​what might be going on, the researchers built a brain environment inside six-millimeter-wide, donut-shaped sponges made of silk protein and collagen. They were populated with stem cells that grew into functional neurons and supporting tissues called glial cells that helped keep the neurons alive and healthy.

When the model’s brain tissue was infected with varicella-zoster alone, there was no sign of an increase in Alzheimer’s signature proteins tau and beta amyloid.

But if the neurons already contain latent herpes simplex virus, exposure to the varicella-zoster virus leads to reactivation of the herpes virus.

This double whammy was followed by a dramatic increase in tau and beta-amyloid proteins associated with Alzheimer’s disease, as well as a slowing of neuronal signaling.

“It’s a one-two punch of two viruses that are very common and usually harmless, but lab tests show that if a new exposure to the varicella-zoster virus wakes up the dormant herpes simplex virus, they can cause problems,” says lead author, biomedical engineer Dana Kearns of Tufts University.

Beta-amyloid proteins can collect in the brain as plaques, which are abnormal groups of protein fragments that disrupt nerve signaling. Tau is a protein that normally keeps microtubules in straight lines. In people with dementia, tau becomes defective and microtubules begin to twist and tangle, starving cells for nutrients.

Exactly how these two proteins might be linked to Alzheimer’s disease is itself a matter of ongoing debate, with drugs targeting plaque formation failing to meet expectations. Yet the fact that they are a feature of the condition makes them a clear signal that something has gone wrong.

Some experts not involved in the study cautioned that the experiment does not definitively demonstrate that this interaction is the cause of Alzheimer’s disease, because building brain tissue outside the human body is a rather artificial environment.

They argue that it is the inflammation, a byproduct of the viral infection, and not the specific virus itself that causes the problem, so other viruses may be just as involved in the disease.

“These are laboratory findings and do not directly implicate these viruses as the main cause of Alzheimer’s disease, but the results are important and should continue to drive research,” said Paresh Malhotra, a neuroscientist at Imperial College London.

Future studies will almost certainly reveal the roles that viruses play in the complex series of events that lead to the degeneration of nerves responsible for Alzheimer’s symptoms.

“We know there’s a link between HSV-1 and Alzheimer’s disease, and some have suggested that the varicella-zoster virus is involved, but what we didn’t know was the sequence of events that viruses set up to drive the disease,” says biomedical engineer David Kaplan of Tufts University and senior author of the paper.

“We believe we already have evidence of these events.

This article was published in the Journal of Alzheimer’s Disease.

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