Alzheimer’s May Be Linked To A Common Virus

People usually catch the virus that causes cold sores in childhood, and it stays in their body for life, hiding quietly in the nerves. Occasionally, triggers like stress, illness, or injury can reactivate it, causing cold sores in some individuals.

However, this very virus — known as herpes simplex virus type 1 — might also be a key factor in a much more serious condition: Alzheimer’s disease.

More than 30 years ago, my team and I made a surprising discovery: the cold sore virus can exist in the brains of elderly individuals.

How a Common Virus and a Risk Gene May Team Up in the Brain

This was the first strong evidence that a virus could silently reside in the brain, which was once believed to be entirely free of germs due to the protective “blood-brain barrier.”

We then uncovered something even more remarkable: individuals with a specific version of a gene called APOE-e4 — which raises the risk of Alzheimer’s — face a significantly higher risk if they’re also infected with this virus.

To dig deeper, we infected brain cells with the virus and found that they generated the same abnormal proteins — amyloid and tau — that are present in the brains of individuals with Alzheimer’s.

How Aging May Awaken a Hidden Viral Threat to the Brain

We think the virus, remains mostly inactive in the body for many years—possibly decades. But as the immune system weakens with age, the virus can reach and reactivate in the brain, damaging brain cells and triggering inflammation.

Over time, repeated reactivations may cause cumulative damage that contributes to Alzheimer’s in some individuals.

Later, we discovered the virus’s DNA within the sticky protein clumps found in the brains of Alzheimer’s patients. Even more promising, antiviral drugs reduced this damage in lab studies, hinting that such treatments might one day slow or even prevent the disease.

Supporting this, large-scale population studies showed that severe infections with the cold sore virus strongly predicted Alzheimer’s risk—and that specific antiviral treatments reduced that risk.

Our investigation continued as we began to question whether other dormant viruses in the body—like the one that causes chickenpox and shingles—might have similar effects.

The shingles vaccine provides an additional hint

When we analyzed health records from hundreds of thousands of people in the UK, we noticed an intriguing pattern: those who had shingles showed only a slightly increased risk of dementia, but individuals who received the shingles vaccine were actually less likely to develop dementia at all.

A new study led by Stanford University found similar results.

This reinforced our long-standing theory that preventing common infections could help reduce the risk of Alzheimer’s. In line with this, other studies showed that infections do increase risk, while certain vaccines appear to offer protection.

We also looked into how known Alzheimer’s risk factors—like infections and head injuries—might reactivate dormant viruses in the brain.

Using a sophisticated 3D brain model with a latent herpes infection, we found that introducing other infections or mimicking a brain injury reactivated the virus, leading to brain damage similar to that seen in Alzheimer’s.

However, when we applied a treatment to reduce inflammation, the virus remained dormant and the damage was prevented.

All of this points to the possibility that the cold sore virus may play a significant role in the development of Alzheimer’s, particularly in individuals with specific genetic risk factors. It also highlights promising new avenues for prevention—like vaccines or antiviral therapies that keep the virus dormant and protect the brain.

What started as a connection between cold sores and memory problems has evolved into a broader and more compelling story—one that could help us better understand and potentially lower the risk of one of the most devastating diseases of our era.

Read the original article on: Sciencearlert

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