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Common vaccinations may be a way to reduce the risk of developing dementia: ScienceAlert

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One in nine Americans age 65 and older will have Alzheimer’s disease by 2022, and countless others will be indirectly affected as caregivers, health care providers and taxpayers.

There is currently no cure – available treatments focus primarily on prevention, encouraging protective factors such as exercise and a healthy diet, and reducing aggravating factors such as diabetes and high blood pressure.

One such aggravating factor is viral infections. Researchers have identified that certain viruses, such as herpes simplex virus type 1 (HSV-1, which causes cold sores), varicella zoster virus (VZV, which causes chickenpox and shingles), and SARS-CoV-2 (which causes COVID-19) can lead to a higher risk of Alzheimer’s disease and dementia after infection.

Figuring out how and when these viruses contribute to disease could help scientists develop new therapies to prevent dementia. However, researchers have failed to consistently detect suspected viruses in the brains of people who have died of Alzheimer’s.

Because the Alzheimer’s disease process can begin decades before symptoms appear, some researchers have proposed that viruses act early in a “run over” fashion; they set off a cascade of events that lead to dementia, but they’ve already taken off. In other words, by the time researchers analyze the patients’ brains, all detectable viral components are gone and the cause is difficult to establish.

We are a team of neurovirologists, neurologists and neuroscientists interested in the role viruses play in neurodegenerative diseases. In our recently published research, we used new technology to look for traces of these viruses in Alzheimer’s patients.

By focusing on the brain’s most vulnerable entry point, the nose, we uncovered a genetic network that provides evidence for a robust viral response.

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Focus on the olfactory system

Many of the viruses implicated in dementia, including herpesviruses and the virus that causes COVID-19, enter the nose and interact with the olfactory system.

The olfactory system is constantly bombarded with odors, pollutants and pathogens. Particles inhaled through the nostrils bind to specific olfactory receptor cells in the tissue lining the nasal cavity.

These receptors send messages to other cells in what is called the olfactory bulb, which acts as a relay station that transmits these messages along the long nerves of the olfactory tract. These messages are then transferred to the area of ​​the brain responsible for learning and memory, the hippocampus.

The hippocampus plays a critical role in assigning contextual information to odors, such as the danger of the bad smell of propane or the comfort of the smell of lavender. This area of ​​the brain is also dramatically damaged in Alzheimer’s disease, causing devastating learning and memory deficits.

For up to 85% to 90% of Alzheimer’s patients, loss of smell is an early sign of the disease.

The mechanism that leads to the loss of smell in Alzheimer’s disease is relatively unknown.

Like muscles that atrophy from lack of use, sensory deprivation is thought to lead to atrophy of brain regions that specialize in interpreting sensory information. Strong sensory input to these regions is critical to maintaining overall brain health.

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Olfactory inflammation and Alzheimer’s disease

We hypothesize that lifelong viral infections are contributors and potential drug targets in Alzheimer’s disease. To test this idea, we used cutting-edge emerging technology to investigate the mRNA and protein networks of the olfactory system of patients with Alzheimer’s disease.

The body uses mRNA, which is transcribed from DNA, to translate genetic material into proteins. The body uses specific mRNA sequences to produce a network of proteins that are used to fight certain viruses.

In some cases, the body continues to activate these pathways even after the virus is cleared, leading to chronic inflammation and tissue damage. Identifying which mRNA sequences and protein networks are present may allow us to infer, to some extent, whether the body is or was responding to a viral pathogen at some point in time.

Previously, sequencing mRNA in tissue samples was difficult because the molecules degraded so quickly. However, new technology specifically addresses this problem by measuring small subsections of mRNA at a time, rather than trying to reconstruct the entire mRNA sequence at once.

We leveraged this technology to sequence mRNA from the olfactory bulb and olfactory tract samples from six people with familial Alzheimer’s, an inherited form of the disease, and six people without Alzheimer’s. We focus on familial Alzheimer’s because there is less variability in the disease than in the sporadic or non-familial form of the disease, which can result from many different individual and environmental factors.

In Alzheimer’s familial samples, we found altered gene expression indicating signs of a past viral infection in the olfactory bulb, as well as inflammatory immune responses in the olfactory tract. We also found higher levels of proteins involved in demyelination in the olfactory tract of familial Alzheimer samples than in controls.

Myelin is a protective fatty layer around nerves that allows electrical impulses to move quickly and smoothly from one area of ​​the brain to another. Damage to myelin blocks signal transduction, resulting in impaired neural communication and, by extension, neurodegeneration.

Based on these findings, we hypothesize that viral infections and the resulting inflammation and demyelination in the olfactory system may disrupt hippocampal function, impairing olfactory bulb communication. This scenario may contribute to the accelerated neurodegeneration seen in Alzheimer’s disease.

Implications for the patient’s health

Epidemiological data support the role of viral infections in the development of Alzheimer’s disease. For example, the varicella zoster virus is associated with an almost three-fold increased risk of developing dementia within five years of infection in patients with a rash on the face.

A recent report also found an almost 70% higher risk of being diagnosed with Alzheimer’s within a year of a COVID-19 diagnosis for people over age 65.

These studies suggest that vaccination may be a potential measure to prevent dementia. For example, vaccination against the seasonal flu virus and shingles is associated with up to a 29% and 30% reduction in the risk of developing dementia, respectively.

More research investigating how viral infections can trigger neurodegeneration could help in the development of antiviral drugs and vaccines against the viruses implicated in Alzheimer’s disease.The conversation

Andrew Bubak, Research Assistant Professor of Neurology, University of Colorado Anschutz Medical Campus; Diego Restrepo, Professor of Cellular and Developmental Biology, University of Colorado Anschutz Medical Campus, and Maria Nagel, Professor of Neurology and Ophthalmology, University of Colorado Anschutz Medical Campus

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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