A new study claims that two common viruses trigger Alzheimer's

The existence of two viruses at the same time can induce an excess of proteins responsible for the distinctive brain plaques associated with Alzheimer's disease, researchers say.
Baba Tamim
Neurons in Alzheimer's disease. 3D illustration showing amyloid plaques in brain tissue, neurofibrillary tangles and distruction of neuronal networks
Neurons in Alzheimer's disease. A 3D illustration showing amyloid plaques in brain tissue, neurofibrillary tangles and distruction of neuronal networks


A group of researchers has claimed that chickenpox and herpes viruses can team up to cause Alzheimer's.

An experiment on model brains added more evidence to the hypothesis that the viruses responsible for chickenpox and herpes can team up to cause Alzheimer's disease, according to a report published in ScienceAlert on Tuesday.

"It's a one-two punch of two viruses that are very common and usually harmless," said the study's lead author, Dana Cairns, a biomedical engineer at Tufts University, Massachusetts.

"But the lab studies suggest that if a new exposure to varicella-zoster virus wakes up dormant herpes simplex virus, they could cause trouble."

Although this argument is still heavily contested, researchers at Tufts University and The University of Oxford stated that the existence of two viruses at the same time can induce an excess of proteins responsible for the distinctive brain plaques associated with Alzheimer's disease, according to researchers.

This paper was published in the Journal of Alzheimer's Disease.

Experiment with doughnut-shaped sponges as brains

The scientists created a brain-like environment within six-millimeter-wide doughnut-shaped sponges made of silk protein and collagen to better understand what was going on.

These were populated with stem cells that developed into functional neurons and supporter tissues known as glial cells, which assisted in keeping the neurons alive and well.

There were no increase in the signature Alzheimer's proteins tau and beta-amyloid when the model brain tissue was infected with varicella-zoster alone. However, if the neurons already contained a dormant herpes simplex virus, exposure to the varicella-zoster virus caused the herpes virus to reactivate.

This double attack was followed by a significant increase in the tau and beta-amyloid proteins linked to Alzheimer's disease and a slowing of neuronal signals.

In the brain, beta-amyloid proteins can form plaques, abnormal clusters of protein fragments that disrupt nerve signaling. Tau is a protein that helps microtubules stay in straight lines. Tau becomes faulty in dementia patients, and microtubules begin to twist and tangle, starving cells of nutrients.

"We know there is a correlation between HSV-1 and Alzheimer's disease, and some suggested involvement of varicella-zoster virus, but what we didn't know is the sequence of events that the viruses create to set the disease in motion," said David Kaplan, a biomedical engineer at Tufts University and the senior author of the paper.

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"We think we now have evidence of those events."

The exact role of these two proteins in Alzheimer's disease is still being debated, with drugs targeting plaque formation falling short of expectations. The fact that they are a feature of the condition clearly indicates that something has gone wrong.

The link

Herpes simplex virus type 1 (HSV-1) and Alzheimer's disease may be related. In addition to being present in large quantities in the brains of the elderly, HSV-1 has been linked to an increased risk of Alzheimer's disease in persons who also carry the gene for the disease.

Varicella-zoster, the chicken pox virus that causes shingles, has a similar ability to the herpes virus to remain dormant in nerve cells for years.

Shingles are painful acute inflammation of the nerve ganglia, with a skin eruption often forming a girdle around the middle of the body. The same virus causes it as chickenpox.

Although shingles seldom occur more than once or twice in a lifetime, the ensuing inflammation may increase the risk of dementia. It was thought to be insufficient to cause Alzheimer's.

However, there are good reasons to believe the two conditions are linked, as per the paper.

Vaccination against the reemergence of the varicella-zoster virus as shingles, for example, showed in population studies in Taiwan, the United Kingdom, South Korea, and the United States to reduce the risk of dementia.

Other experts caution

Some experts who were not involved in the study cautioned that the experiment does not prove that this interaction causes Alzheimer's disease because creating brain-like tissue outside the human body is a fairly artificial environment.

They argue that the problem is caused by inflammation, a byproduct of viral infection, rather than the virus itself, and that other virus could 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 stimulate research," said Paresh Malhotra, a neurologist at the Imperial College London.

Study abstract:

Background:Varicella zoster virus (VZV) has been implicated in Alzheimer’s disease (AD), and vaccination against shingles, caused by VZV, has been found to decrease the risk of AD/dementia. VZV might reside latently in brain, and on reactivation might cause direct damage leading to AD, as proposed for herpes simplex virus type 1 (HSV-1), a virus strongly implicated in AD. Alternatively, shingles could induce neuroinflammation and thence, reactivation of HSV-1 in brain. Objective:To investigate these possibilities by comparing the effects of VZV and HSV-1 infection of cultured cells, and the action of VZV infection on cells quiescently infected with HSV-1. Methods:We infected human-induced neural stem cell (hiNSC) cultures with HSV-1 and/or VZV and sought the presence of AD-related phenotypes such as amyloid-β (Aβ) and P-tau accumulation, gliosis, and neuroinflammation. Results:Cells infected with VZV did not show the main AD characteristics, Aβ and P-tau accumulation, which HSV-1 does cause, but did show gliosis and increased levels of pro-inflammatory cytokines, suggesting that VZV’s action relating to AD/dementia is indirect. Strikingly, we found that VZV infection of cells quiescently infected with HSV-1 causes reactivation of HSV-1 and consequent AD-like changes, including Aβ and P-tau accumulation. Conclusion:Our results are consistent with the suggestion that shingles causes reactivation of HSV1 in brain and with the protective effects against AD of various vaccines, as well as the decrease in herpes labialis reported after certain types of vaccination. They support an indirect role for VZV in AD/dementia via reactivation of HSV-1 in brain.

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