Alzheimer’s disease can begin almost unnoticed, often disguised in the first few months or years as the forgetfulness common to older adults. What causes the disease remains largely a mystery.
But researchers at Tufts University and Oxford University, using three-dimensional human tissue culture models that mimic the brain, have shown that usually The varicella-zoster virus (VZV), which causes chickenpox and shingles, may activate another common virus, herpes simplex virus (HSV), to initiate the early stages of Alzheimer’s disease.
Normally HSV-1 (one of the main variants of the virus) is dormant within the neurons of the brain, but When activated, it leads to the accumulation of tau and amyloid beta proteins and neuronal loss of function — features found in Alzheimer’s patients.
“Our results suggest that one pathway of Alzheimer’s disease, a disease caused by VZV infection, is There are inflammatory triggers that wake up HSV in the brain,” said Dana Cairns, GBS12 Research Associate in the Department of Biomedical Engineering. “While we demonstrated a link between VZV and HSV-1 activation, other inflammatory events in the brain may also awaken HSV-1 and contribute to Alzheimer’s disease.”
The study was published in The Journal of Alzheimer’s Disease superior
latent virus
“We have been Research has overwhelmingly established evidence that HSV is associated with an increased risk of Alzheimer’s disease in patients,” said David Kaplan, chair of the Tufts School of Engineering’s Department of Biomedical Engineering and the Stern Family Professor of Engineering. One of the first to hypothesize a link between the herpes virus and Alzheimer’s disease was Ruth Itzhaki of the University of Oxford, who collaborated with the Kaplan lab on the research.
“We know there is a correlation between HSV-1 and Alzheimer’s disease, and some believe that VZV is involved , but we don’t know the sequence of events that the virus creates to cause disease in motion,” he said. “We think we now have evidence of these events.”
An estimated 3.7 billion people, according to the World Health Organization At the age of 50 people were infected with HSV-1, the virus that causes oral herpes. In most cases, it is asymptomatic and lies dormant within nerve cells.
When activated, it causes inflammation of the nerves and skin, leading to painful open sores and blisters. Most carriers — one in two Americans, according to the Centers for Disease Control and Prevention — will have very mild to no symptoms before the virus goes dormant.
The varicella-zoster virus is also very common, and about 95% of people are infected by the age of 20. Many of these cases presented with chickenpox. VZV, a form of the herpes virus, can also stay in the body and find its way into nerve cells before going dormant.
Later in life, VZV can reactivate to cause shingles, a disease characterized by the formation of Blisters and nodules in a band-like pattern and can be very painful for weeks or even months. One in three people will eventually develop shingles in their lifetime.
Link between HSV-1 and Alzheimer’s disease only when HSV-1 is reactivated to cause ulcers, This happens when blisters and other painful inflammatory conditions occur.
How the sleeping virus woke up
To better understand viruses and Alzheimers The cause-and-effect relationship between Haimer’s disease, Tufts University researchers, consists of silk protein and collagen.
They filled the sponge with neural stem cells that grew and became functional neurons capable of transmitting to each other for a short period of time Signal networks, as they do in the brain. Some stem cells also form glial cells, which are normally found in the brain and help keep neurons alive and functioning.
Neurons growing in brain tissue may be infected with VZV, but this alone does not cause The Alzheimer’s hallmark proteins tau and beta-amyloid form — components in the brains of Alzheimer’s patients — and neurons continue to function normally.
However, if neurons already carry quiescent HSV-1, exposure to VZV results in HSV reactivation, tau and β- Amyloid increased dramatically, and neuronal signaling began to slow.
“This is one-half of two very common and generally harmless viruses, but laboratory studies have shown that If new exposure to VZV wakes up dormant HSV-1, they can cause trouble,” Cairns said.
“This is that other infections and other causal pathways may still lead to Alzheimer’s disease, while head trauma, obesity Or risk factors such as alcohol consumption suggest that they may cross over to each other when HSV reappears in the brain,” she added.
The researchers observed that VZV-infected samples started producing higher levels of cytokines that are normally involved in triggering Inflammation. In many clinical cases, VZV is known to cause brain inflammation, which may lead to activation and increased inflammation of dormant HSV, Kaplan noted.
Repeated cycle of HSV-1 activation can lead to more inflammation, plaque buildup in the brain and the accumulation of neuronal and cognitive impairments.
The VZV vaccine – used to prevent chickenpox and shingles – has also been shown to significantly reduce dementia risks of. Vaccines may help stop the cycle of viral reactivation, inflammation and neuronal damage.
The researchers also point to the long-term neurological effects that some COVID patients experience from the SARS-CoV-2 virus, especially in In older adults, both VZV and HSV-1 can be reactivated after COVID infection. In these cases, close attention is recommended for possible subsequent cognitive effects and neurodegeneration, they said.
More information: Dana M. Cairns et al., Varicella-zoster virus may be involved in Alzheimer’s disease through reactivation of quiescent herpes simplex virus type 1, Alzheimer’s disease Magazine (2022). DOI: 10.3233/JAD-220287
Citation : Common Viruses May Trigger Alzheimer’s Disease Attacks ( July 29, 2022), retrieved August 28, 2022, from https://medicalxpress.com/news/2022-07-common-viruses-triggering-onset-alzheimer. html
This document is protected by copyright. Except for any fair dealing for private study or research purposes, no part may be reproduced without written permission. The content is for reference only.
