Dementia can be the result of a viral infection and can be cured by vaccination

In 2022, one in nine Americans aged 65 and over had Alzheimer's disease, the most common form of dementia. Recent studies have shown that a relatively harmless virus that causes herpes may play a role in causing the disease. Dailymail.

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Hundreds of billions of dollars have been spent on futile attempts to cure dementia, one of the world's leading causes of death. In the past, much attention has been paid to drugs that clear up clumps of proteins associated with a disorder in the brain or slow down the severe cognitive decline that sufferers suffer.

But a growing body of research suggesting viruses may contribute to Alzheimer's disease has led experts to question whether vaccines can help stop the disease before it occurs.

The link between viruses and dementia is not entirely new.

Studies have repeatedly shown that people vaccinated against other viruses have a lower risk of developing dementia.

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For example, limited evidence suggests that flu shots reduce the risk of dementia by up to 29 percent, while the herpes zoster vaccine (shingles vaccine) reduces the risk by 30 percent.

Experts believe that Alzheimer's disease is associated with the accumulation of beta-amyloid proteins in the brain, which stick together and cause damage to key neurons, causing characteristic symptoms such as memory impairment and loss of overall cognitive function.

The uncontrolled growth of amyloid plaques causes massive cell death, which leads to a rapid deterioration in the condition of patients.

But there is some uncertainty about whether plaque buildup is the cause or one of the symptoms of dementia.

There are drugs to treat Alzheimer's disease by reducing the production of amyloid. But it hasn't worked so far, according to Diego Restrepo, a professor of cell biology at the University of Colorado. And even if drugs remove some of the amyloid plaque, it's hard to reverse the damage already done to the brain.

By studying amyloid plaques, scientists found that they have antiviral properties, which led them to believe that this could be a way to protect the brain from infections.

“We think the virus itself can cause these amyloid plaques to build up to the point where you have clinical symptoms of dementia,” said Maria Nagel, a professor of neurology and ophthalmology at the University of Colorado.

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Over time, over decades, and as we encounter various infections, amyloid plaques build up to the point where they prevent brain cells from communicating with each other, triggering a cascade of memory problems.

“So one thought is that you can prevent deposits from building up before it gets so bad that you develop dementia. We think this is an early risk factor that will prevent true clinical dementia,” Dr. Nagel said.

The virus is usually inhaled through the nose or mouth, where it enters the nasal cavity and attaches itself to the small olfactory nerve roots that hang down there.

The virus itself then attaches itself to the nerves, which can cause us to lose our ability to smell.

The virus also has access to our brains through the olfactory nerve, where it causes inflammation—another telltale sign of Alzheimer's disease.

“In every brain we've dissected from patients with Alzheimer's disease, we always find a lot of inflammatory cells in the brain. Infections, especially chronic viral infections, can usually trigger an inflammatory response through the immune system. Because your immune system tries to fight the viruses that appear. This creates chronic inflammation,” said Dr. Trinh, chief medical officer of Irvine Clinical Research and a member of the Orange County Alzheimer's Board.

He added: “We know that chronic inflammation is bad for the brain. So I think there's definitely a connection here with chronic infection, inflammation, and Alzheimer's."

According to Dr. Nagel, the most likely pathogens that can affect the brain and cause cognitive decline in older adults are the varicella-zoster varicella-zoster virus and herpes simplex virus type 1 (HSV-XNUMX).

More than 90 percent of US adults are infected with HSV-1, and most of them never get herpes.

“The reason these viruses are suspect is that they are actually dormant or dormant, in a sense, in the neurons in the head region. They have direct access to the nose when they wake up and also to the brain,” said Dr. Nagel.

Other viruses may play a role. HIV can also cause early dementia in patients because it can replicate in the brain and cause some changes, but this is not necessarily Alzheimer's type dementia.

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It's unclear how many cases could be prevented by vaccines, but Andrew Bubak, assistant professor of neurology at the University of Colorado, said, "We always see that number drop by about 28 to 30 percent after the introduction of various vaccines, not just the shingles vaccine." , but also seasonal flu vaccines. It seems that a significant proportion of cases can at least be delayed—perhaps not prevented, but delayed.”

There are currently no HSV-1 vaccines available, but some are being developed.

Dr. Treen said the idea is that we could use vaccines that will prevent people from getting these infections, which in turn will prevent amyloid from building up in the body.

“I think vaccination against viruses is a viable route. I don't think it will cure Alzheimer's because there are multiple paths to Alzheimer's. But I think we have to do everything we can to close all the doors and all the different routes,” he said. “Vaccination against viruses is certainly a good way to go because it works and we can do it right now.”

Researchers are still working on identifying the exact viruses that may have played a role in causing dementia.

This is because the process of dementia can begin years before the onset of symptoms, and so by the time scientists examine the brains of patients, detectable elements of previous viral infections have disappeared and it is difficult to establish a causal relationship.

Therefore, the researchers hypothesized that viruses accelerate the process of cognitive decline that is already taking place.

A University of Colorado study published last December in the journal Neurobiology of Aging found that viruses that damage patients' sense of smell can hasten the onset of Alzheimer's.

Loss of smell is an early sign of the disease in up to 90 percent of Alzheimer's patients. The researchers studied six people with Alzheimer's disease and six people without it. Patients had a hereditary form of Alzheimer's disease, which has less variability. They focused on the nose, as it is the most vulnerable entry point to the brain, and studied samples taken from the patients' olfactory bulb and tract, the lower part of the brain above the nasal cavity, which is responsible for smell.

Samples from Alzheimer's patients showed altered gene expression demonstrating past viral infection in the olfactory bulb as well as inflammatory immune responses in the olfactory tract. The samples also had more proteins that contribute to myelin damage.

Myelin is a protective layer around the nerves that allows electrical impulses to be conducted easily and quickly in the brain. When this layer is disrupted, parts of the brain are also unable to communicate with each other, contributing to an overall decline in cognitive function.

The findings led researchers to believe that viral infections and the resulting inflammation in the olfactory system could prevent the hippocampus in the brain from communicating with the olfactory bulb, which contributes to neurodegeneration and ultimately Alzheimer's disease.

One explanation is that viruses such as herpes cause the accumulation of amyloid, which is a hallmark of Alzheimer's disease.

Another theory is that if infectious bacteria reach the brain, they can activate immune cells in the brain called microglia. In turn, this causes inflammation in the brain, which leads to the death of nerve cells and, ultimately, to the progression of dementia.

In most people, the immune system suppresses the virus of the primary infection before it can have a significant effect on the central nervous system.

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