Alzheimer’s is an incredibly prevalent condition that is affecting more and more adults each year.
Right now, it’s estimated that as many as 5.8 million Americans live with Alzheimer’s , a number that’s expected to nearly triple in the next 30-40 years.
Though the majority of those living with Alzheimer’s are over 65 years old, it’s not uncommon for younger adults to develop the condition.
What’s really problematic, though, is that Alzheimer’s may only be diagnosed too late—by the time symptoms show up enough to cause concern and prompt sufferers to seek out medical help, the deterioration may already be well underway.
One recent study found a surprising cause behind the neuroinflammation that leads to the degenerative brain disease. Understand what triggers the condition may very well be a great step toward figuring out how to treat, cure, and possibly even prevent it!
A team of researchers from Tufts University working together with the University of Oxford  looked at a specific virus, and found that its presence in the body could lead to some serious brain degeneration.
The virus in question is the varicella zoster virus, which is the virus responsible for both shingles and chickenpox. These two childhood diseases were once very common, though modern vaccines have been able to keep their spread under control.
According to the research, the varicella zoster virus, or VSV, has the potential to activate the herpes simplex virus (HSV). One of the HSV’s variants, HSV-1, typically is found in the brain, but in a dormant state. When activated by the VSV, however, it can cause the buildup of both amyloid beta and tau proteins. As research has shown in the past, an accumulation of these proteins is directly linked to a higher risk of Alzheimer’s and dementia because they increase neuroinflammation and contribute to brain deterioration. VSV triggering HSV-1 can actually cause loss of neuronal function, which can elevate your risk—or worsen existing cases—of Alzheimer’s disease.
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Here's a terrifying fact, though: the WHO estimates that roughly 3.7 billion people (nearly half of the world’s population) is living with HSV-1. The virus is typically asymptomatic and remains dormant within nerve cells.
However, when it comes in contact with the VSV virus—which the CDC estimates 95% of people will be infected with before the age of 20—there is a very real chance that the HSV-1 virus will be activated and contribute to brain deterioration and accelerated aging.
There is some good news: according to the research, only a reactivation of the HSV-1 virus is likely to elevate the risk of Alzheimer’s.
When people were exposed to the VSV with no HSV-1 in their brain cells, it didn’t cause the buildup of the amyloid proteins or increase inflammation in the brain. However, if brain neurons are already harboring HSV-1, exposure to VSV will cause the slowdown in neuronal function and the buildup of amyloid proteins.
According to the research, “Repeat cycles of HSV-1 activation can lead to more inflammation in the brain, production of plaques, and accumulation of neuronal and cognitive damage.”
The good news is that there are means of treating and preventing this problem!
HSV-1 viral infection symptoms can be managed using medications (such as acyclovir), though there is no known cure for the infection itself.
Given the statistics mentioned above, it’s incredibly difficult to avoid exposure to the HSV-1 virus. Chances are, like nearly half of the world’s population, you have been infected by the virus, and it’s merely remaining dormant in your body. For most people, there will never or rarely be an outbreak of viral symptoms, but it will merely be a “silent passenger”
The best thing you can do is to take active precautions to avoid exposure to the VSV virus. If you’ve already suffered from chickenpox as a child, you should be safe against re-exposure as an adult. However, if you have never been exposed to the VSV virus, it’s a good idea to take safety measures to avoid it on the off chance that it could re-activate the HSV-1 virus living in your brain and increase the risk of neuroinflammation and brain deterioration.
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