(ORDO NEWS) — Experiments by researchers from the US and the UK have shown what mechanism is involved in this.
The varicella-zoster virus that causes chickenpox and shingles can reactivate dormant herpes simplex virus in brain neurons and spike levels of tau and beta-amyloid proteins, eventually triggering the development of Alzheimer’s disease.
This conclusion was reached by scientists from Tufts University in Massachusetts (USA) and Oxford University (UK), whose results were published in the Journal of Alzheimer’s Disease .
With chickenpox ( Varicella zoster virus ), which spreads by airborne droplets and belongs to the family of herpetic viruses, almost every one of us encountered in childhood: the reactivation of the “sleeping” pathogen causes a maculopapular vesicular skin rash, which is often accompanied by pain and itching.
In three to seven days, it becomes covered with a dry crust and soon disappears completely, occasionally leaving scars. Nevertheless, the virus is able to remain in the body, penetrating the nerve cells and then falling into “hibernation”.
Reactivation in every third case usually occurs at a later age, causing herpes zoster, characterized by unilateral skin rashes with severe pain.
“Our results have shown a pathway to Alzheimer’s disease caused by infection with Varicella zoster virus (VZV), which creates inflammatory triggers that awaken herpes simplex virus 1 (HSV-1) in the brain,” said Dana Cairns, researcher in the Department of Biomedical Engineering at Tufts University.
“While we have demonstrated a link between VZV activation and HSV-1, it is possible that other inflammatory processes in the brain can also awaken HSV-1 and lead to Alzheimer’s disease.”
According to WHO estimates, almost four billion people in the world under the age of 50 are carriers of HSV-1, a common infectious disease of the skin and mucous membranes.
Most often, it hides in nerve cells and does not manifest itself in any way. The link between “activated” herpes simplex virus 1 and Alzheimer’s disease was already known, but the mechanism remained unclear, the researchers said.
To answer this question, the authors of the new work took tiny collagen sponges and used neural stem cells to recreate a three-dimensional model of human tissue culture that mimics the brain.
“We infected cultures of human induced neural stem cells (hiNSC) with HSV-1 and/or varicella-zoster virus and looked for the presence of phenotypes associated with Alzheimer’s disease, such as accumulation of beta-amyloid, tau proteins, gliosis (change in glial cells in response to on damage to the central nervous system and neuroinflammation,” the scientists write.
The grown nerve cells were able to be infected with Varicella zoster virus , but this in itself did not provoke the appearance of markers of Alzheimer’s disease, although the level of cytokines that trigger the inflammatory reaction increased.
However, when the herpes simplex virus 1 was added to the process, exposure to Varicella zoster virus activated it and caused the accumulation of tau-beta-amyloid proteins.
These results also explain why the varicella-zoster virus vaccine reduces the risk of neurodegeneration: presumably, the vaccine helps to stop the reactivation of the virus, the development of inflammation and damage to neurons.
Perhaps a similar mechanism is involved in the strange association between flu vaccination and a 40 percent reduction in the chance of developing Alzheimer’s disease in people over 65 years of age.
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