Scientists from Tufts University and the University of Oxford found that varicella-zoster virus (VZV), which commonly causes chickenpox and shingles, may activate herpes simplex (HSV), another common virus, to trigger the early stages of Alzheimer’s.
The research is published in the Journal of Alzheimer’s Disease and was conducted by Dana Cairns et al.
According to the World Health Organization, an estimated 3.7 billion people under the age of 50 have been infected with HSV-1—the virus that causes oral herpes.
In most cases it is asymptomatic, lying dormant within nerve cells.
When activated, it can cause inflammation in nerves and skin, causing painful open sores and blisters. Most carriers—and that’s one in two Americans—will have between very mild to no symptoms before the virus becomes dormant.
Varicella zoster virus is also extremely common, with about 95 percent of people having been infected before the age of 20. Many of those cases are expressed as chicken pox.
VZV, which is a form of herpes virus, can also remain in the body, finding its way to nerve cells before then becoming dormant.
Later in life, VZV can be reactivated to cause shingles, a disease characterized by blisters and nodules in the skin that form in a band-like pattern and can be very painful, lasting for weeks or even months.
One in three people will eventually develop a case of shingles in their lifetime.
The link between HSV-1 and Alzheimer’s disease only occurs when HSV-1 has been reactivated to cause sores, blisters, and other painful inflammatory conditions.
In the study, the team found that neurons grown in the brain tissue can be infected with VZV, but that alone did not lead to the formation of the signature Alzheimer’s proteins tau and beta-amyloid.
However, if the neurons already harbored quiescent HSV-1, the exposure to VZV led to a reactivation of HSV, and a dramatic increase in tau and beta-amyloid proteins, and the neuronal signals begin to slow down.
The researchers observed that the VZV infected samples started to produce a higher level of cytokines—proteins that are often involved in triggering an inflammatory response.
VZV is known in many clinical cases to cause inflammation in the brain, which could possibly lead to activation of dormant HSV and increased inflammation.
Repeat cycles of HSV-1 activation can lead to more inflammation in the brain, production of plaques, and accumulation of neuronal and cognitive damage.
The results suggest one pathway to Alzheimer’s disease, caused by a VZV infection which creates inflammatory triggers that awaken HSV in the brain.
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