Study: Common viruses can cause Alzheimer’s disease!

Alzheimer’s disease hides for many years before its first symptoms appear, and it often begins in a form of forgetfulness that is common in older people.

Despite various studies and years of research, Alzheimer’s disease, the most common dementia, is still largely a mystery, and scientists still cannot find a cure for it.

But researchers at Tufts and Oxford University, using a 3D human tissue culture model that mimics the brain, have shown that herpes zoster virus (VZV), one of eight herpes viruses that infect people commonly responsible for chickenpox and shingles, can activate herpes simplex (HSV), another common virus, to cause the early stages of Alzheimer’s disease.

Herpes simplex virus 1 (HSV-1), the main variant of the virus, is usually latent in the neurons of the brain, but when activated, it leads to the accumulation of tau and beta-amyloid proteins and loss of neuronal function, which is the hallmark found in patients with Alzheimer’s disease.

Dana Kearns, Associate Research Fellow at the Department of Biomedical Engineering, said: “Our results point to a single pathway for Alzheimer’s disease, varicella-zoster infection, that creates inflammatory triggers that awaken HSV in the brain. While we are demonstrating the link between chickenpox reactivation and HSV-1 simple, it is possible that other inflammatory processes in the brain can also awaken herpes simplex virus-1 (HSV-1) and lead to Alzheimer’s disease.”

David Kaplan, Stern Professor of Engineering and Chair of Biomedical Engineering at the Tufts School of Engineering, said: “We have been working on a lot of compelling evidence that HSV is associated with an increased risk of Alzheimer’s in patients. He was one of the first to hypothesize a link between HSV and Alzheimer’s disease. Ruth Itzaki of the University of Oxford, who collaborated with Kaplan’s lab on this study.”

He continued: “We know there is a link between herpes simplex virus 1 and Alzheimer’s disease, and some have suggested the involvement of the herpes zoster virus, but what we didn’t know was the sequence of events that create the viruses to cause the disease. We believe we now have evidence of those events.”

According to the World Health Organization, about 3.7 billion people under the age of 50 are infected with HSV-1, the virus that causes oral herpes. In most cases, it is asymptomatic and lies dormant in neurons.

When activated, it can cause inflammation of the nerves and skin, causing painful open sores and blisters. Most carriers of the virus will have very mild or no symptoms before the virus becomes latent.

The varicella-zoster virus is very common, affecting about 95% of people under the age of 20. Shingles, a form of the herpes virus, can also remain in the body, finding its way into nerve cells before it becomes dormant.

Later in life, the varicella-zoster virus can reactivate, causing herpes zoster, a disease characterized by blistering and rash that can be very painful and last for weeks or even months. One in three people will eventually develop shingles in their lifetime.

The link between HSV-1 and Alzheimer’s only occurs when HSV-1 is reactivated, causing ulcers, blisters, and other painful inflammatory conditions.

How dormant viruses wake up

To better understand the causal relationship between viruses and Alzheimer’s disease, researchers at Tufts University recreated a brain-like environment in a 6mm-wide pie-shaped sponge made from silk proteins and collagen.

They fill the sponge with neural stem cells, which turn into functional neurons that can signal to each other over a network, just like in the brain.

Some stem cells also form glial cells, which are normally found in the brain and help keep nerve cells alive and functioning.

They found that neurons growing in brain tissue can get chickenpox, but this by itself did not lead to the formation of separate Alzheimer’s proteins, tau and beta-amyloid, which are formed in Alzheimer’s disease patients’ brains, and that neurons continued normally. function. .

However, if neurons already contained resting HSV-1, exposure to herpes zoster resulted in herpes simplex reactivation, a significant increase in tau and beta-amyloid proteins, and nerve signals began to slow down.

Kearns says laboratory studies show that if new exposure to shingles activates dormant HSV-1, it could cause problems.

The researchers noticed that samples infected with the varicella-zoster virus began to produce higher levels of cytokines, proteins often involved in triggering the inflammatory response. Kaplan noted that the herpes simplex virus is known to cause inflammation in the brain in many clinical cases, which can lead to the activation of the dormant herpes simplex virus and increased inflammation.

Repeated cycles of HSV-1 activation can lead to increased inflammation in the brain, plaque formation, and accumulation of neurological and cognitive impairment.

The varicella-zoster virus vaccine has also been shown to significantly reduce the risk of dementia. It is possible that the vaccine helps to stop the virus reactivation cycle, inflammation and damage to nerve cells.

Source: Medical Express