Good news! However, these results are based on a 3D brain model not in vivo! Are you vaccinated against shingles and is your last vaccination still effective?
About 8% of human DNA is made up of virus DNA. Why should viruses not be involved in neurodegenerative diseases like Alzheimer's.
".... study ... has found two common viruses may be working in tandem to trigger the earliest stages of Alzheimer’s disease. The findings build on a growing body of evidence implicating the herpes virus in neurodegenerative disease. ...
Considering more than two-thirds of the world’s population carry herpes simplex virus type I (HSV-1), there must be other factors that reactivate the dormant virus and trigger this cascade of events that lead to Alzheimer’s. ...
the research found exposing brain cells harboring dormant HSV-1 to VZV [varicella zoster virus] led to a reactivation of the herpesvirus and a cascade of the toxic plaques known to be signs of Alzheimer’s. However, all of these Alzheimer’s signs did not appear when brain cells were exposed to VZV in the absence of herpesvirus. ...
The study also speculates potential future Alzheimer’s problems may arise from the COVID-19 pandemic as SARS-CoV-2 infections have been known to reactivate dormant VSV and HSV-1 infections. ..."
Considering more than two-thirds of the world’s population carry herpes simplex virus type I (HSV-1), there must be other factors that reactivate the dormant virus and trigger this cascade of events that lead to Alzheimer’s. ...
the research found exposing brain cells harboring dormant HSV-1 to VZV [varicella zoster virus] led to a reactivation of the herpesvirus and a cascade of the toxic plaques known to be signs of Alzheimer’s. However, all of these Alzheimer’s signs did not appear when brain cells were exposed to VZV in the absence of herpesvirus. ...
The study also speculates potential future Alzheimer’s problems may arise from the COVID-19 pandemic as SARS-CoV-2 infections have been known to reactivate dormant VSV and HSV-1 infections. ..."
"... But researchers ... using a three-dimensional human tissue culture model mimicking the brain, have shown that varicella zoster virus (VZV), which commonly causes chickenpox and shingles, may activate herpes simplex (HSV), another common virus, to set in motion the early stages of Alzheimer’s disease. ...
Normally HSV-1 – one of the main variants of the virus - lies dormant within the neurons of the brain, but when it is activated it leads to accumulation of tau and amyloid beta proteins, and loss of neuronal function ...
Varicella zoster virus is also extremely common, with about 95 percent of people having been infected before the age of 20. ...
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. ..."
Normally HSV-1 – one of the main variants of the virus - lies dormant within the neurons of the brain, but when it is activated it leads to accumulation of tau and amyloid beta proteins, and loss of neuronal function ...
Varicella zoster virus is also extremely common, with about 95 percent of people having been infected before the age of 20. ...
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. ..."
From the 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."
Common viruses may be triggering the onset of Alzheimer’s disease Shingles infection may activate dormant neurological herpes viruses, causing inflammation and accumulation of Alzheimer’s associated proteins in the brain
Potential Involvement of Varicella Zoster Virus in Alzheimer’s Disease via Reactivation of Quiescent Herpes Simplex Virus Type 1 (no public access)
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