A startling new study reveals common viruses may trigger the onset of Alzheimer’s disease. Researchers from Tufts University and the University of Oxford say that the varicella zoster virus (VZV), which causes chickenpox and shingles, may activate herpes simplex (HSV), to set in motion the early stages of Alzheimer’s.
HSV-1 usually lies dormant within the brain’s neurons, but when activated, it leads to accumulation of tau and amyloid beta proteins, and loss of neuronal function, which are signature features found in Alzheimer’s patients.
“Our results suggest one pathway to Alzheimer’s disease, caused by a VZV infection which creates inflammatory triggers that awaken HSV in the brain,” says Dana Cairns, a research associate in the Biomedical Engineering Department at Tufts University, in a media release. “While we demonstrated a link between VZV and HSV-1 activation, it’s possible that other inflammatory events in the brain could also awaken HSV-1 and lead to Alzheimer’s disease.”
David Kaplan, chair of the Department of Biomedical Engineering at Tufts’ School of Engineering, says they now have proof of the sequence of events that the viruses create for the onset of Alzheimer’s.
“We have been working off a lot of established evidence that HSV has been linked to increased risk of Alzheimer’s disease in patients,” explains Kaplan. “We know there is a correlation between HSV-1 and Alzheimer’s disease, and some suggested involvement of VZV, but what we didn’t know is the sequence of events that the viruses create to set the disease in motion. We think we now have evidence of those events.”
For the study, researchers recreated brain-like environments in 6 millimeter-wide donut-shaped sponges made of silk protein and collagen in a 3D human tissue culture model. The sponges were inhabited with neural stem cells that grow and become functional neurons capable of passing signals to each other in a network, just like they do in the brain.
Researchers say neurons grown in the brain tissue can be infected with VZV, but that didn’t lead to the formation of the tau and beta-amyloid proteins and that the neurons continued to function normally. However, if the neurons already housed HSV-1, the exposure to VZV led to an HSV reactivation, and a drastic increase in tau and beta-amyloid proteins. The neuron signals then began to slow down.
“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,” notes Cairns. “It’s still possible that other infections and other pathways of cause and effect could lead to Alzheimer’s disease, and risk factors such as head trauma, obesity, or alcohol consumption suggest they may intersect at the re-emergence of HSV in the brain.”
VZV-infected samples produced a higher level of cytokines — proteins which are involved in triggering an inflammatory response. Kaplan says VZV is known to cause inflammation in the brain, which could activate dormant HSV and increase inflammation.
Researchers note that “repeat cycles of HSV-1 activation can lead to more inflammation in the brain, production of plaques, and accumulation of neuronal and cognitive damage.”
A VZV vaccine, which prevents chickenpox and shingles, has also reduced the risk of dementia. Researchers say it’s possible the VZV vaccine helps stop the cycle of viral reactivation, inflammation and neuronal damage.
The study is published in the Journal of Alzheimer’s Disease.