
THIS simple antiviral can lower the risk of Alzheimer's
In 2020 alone, the disease cost the US more than $300 billion in care and related expenses.
Despite decades of research, the root cause of Alzheimer's remains unclear. What is known, though, is that abnormal protein deposits in the brain, especially amyloid-beta plaques and tau tangles, play a significant role in its development. But why these plaques form in the first place is a question science is still chasing.
Research suggests that a common virus, herpes simplex virus type 1 (HSV-1), might be involved in triggering these damaging brain changes.
It's the same virus responsible for cold sores. At first, this sounds surprising. But as studies begin to piece together more evidence, the idea is gaining ground.
The cold sore virus and the brain
HSV-1 is extremely common. According to the
World Health Organisation
, nearly 64% of people under the age of 50 carry the virus. Often, it stays hidden in the body, showing up now and then as cold sores. But here's where things get interesting: HSV-1 is a neurotropic virus; it can invade and remain dormant in nerve cells, including those in the brain.
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Back in the 1990s,
Professor Ruth Itzhaki
was one of the first to spot HSV-1 DNA inside Alzheimer's brain plaques. Her research also found that people with a genetic risk factor were more vulnerable to the virus's effects in the brain.
Fast forward 30 years, and
new studies
are similar to her findings. Recent lab experiments show HSV-1 can trigger the buildup of amyloid-beta, one of the hallmark features of Alzheimer's. The idea is that repeated reactivation of the virus may damage neurons and kickstart brain inflammation, slowly increasing the risk of dementia-like decline over time.
Numbers add a new layer to the theory
A new study led by Gilead Sciences and the University of Washington brings real-world data into the conversation. Using medical records from over 215 million Americans, the researchers looked at whether those with an HSV-1 diagnosis were more likely to develop Alzheimer's, and whether antiviral medications made a difference.
Here's what the numbers showed:
People with HSV-1 had an 80% higher risk of developing Alzheimer's compared to those without it.
Those who received antiviral treatment had about a 17% lower risk of Alzheimer's compared to untreated individuals.
This large-scale study offers something many previous ones lacked: population-wide evidence that supports earlier lab-based theories. But it's not without flaws. The data came from insurance claims, which means many mild or undiagnosed HSV-1 cases likely went unnoticed. Also, the specifics, such as the type, dose, or duration of antivirals, were not available.
These gaps leave room for caution when interpreting the results.
It's tempting to jump to conclusions, but science moves slowly and carefully. The connection between HSV-1 and Alzheimer's is still correlational, meaning that while patterns are visible, they don't prove cause and effect.
There are many possible explanations. For example, HSV-1 may not directly cause Alzheimer's but might trigger immune system changes, especially in genetically susceptible people. Or, people with weaker immune defences might be more prone to both HSV-1 reactivations and neurodegenerative decline.
What complicates things further is that Alzheimer's is influenced by many factors:
Age is still the biggest risk.
Genetics, like the APOE ε4 gene, play a key role.
Lifestyle factors such as smoking, poor diet, and lack of physical activity also contribute.
And now, chronic infections like HSV-1 may be another layer of the puzzle.
In short, no single cause has been found, but pieces like this help build a clearer picture.
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