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Amyloid beta plaques and tau illustration. (NIH Image Gallery/Flickr/CC BY-NC 2.0)

We Now Have Even More Evidence That Herpes Could Trigger Alzheimer's Disease

The brain is such an intricate system.

DAVID NIELD
13 JUL 2018
 

We know about the devastating effects of Alzheimer's, but scientists still aren't certain about how it gets started. New research lends credence to an older idea, that bacteria and viruses could be contributing to the root causes of the brain disease.

 

In this latest study, the association has only been spotted in mice and petri dishes, but it's still a significant finding.

When infected with herpes viruses, previously linked to Alzheimer's, neurons in both the mice and the lab tests quickly developed amyloid beta (Aβ) plaques – thought to lead to Alzheimer's.

The scientists behind the study are suggesting that the plaque build-up might be the result of some kind of defence mechanism put in place by the body, as it tries to protect itself from attack.

Those sticky buildups of proteins then start damaging the connections between brain cells rather than guarding them.

For years, questions have been asked about how the onset of Alzheimer's is linked to the amyloid beta plaques found in the brains of those who have the disease. This new research further bolsters the hypothesis that the herpes virus is somehow involved.

"Our findings reveal a simple and direct mechanism by which herpes infections trigger the deposition of brain amyloid as a defense response in the brain," explains one of the researchers, Rudolph Tanzi from the MassGeneral Institute for Neurodegenerative Disease (MIND).

 

"In this way, we have merged the infection hypothesis and amyloid hypothesis into one Antimicrobial Response Hypothesis of Alzheimer's disease."

Based on past research, the scientists chose herpes simplex 1 (HSV-1) and herpesvirus 6 (HHV-6) as likely contenders for an Alzheimer's link – HSV-1 is the virus that causes cold sores, by the way.

Not only did experiments show virus infections leading to more deposits of amyloid beta, mice bred with human-like Aβ were better able to fend off the damage of HSV-1, suggesting these proteins are indeed some kind of counter-attack measure.

That idea – that these plaques are trying to stop the brain getting infected – isn't a completely new one, but it's now looking even more plausible.

It also matches up with research published just a few weeks ago, showing higher levels of herpes viruses in the brains of people who have died with Alzheimer's.

"It's possible that chronic infection with pathogens like herpes that remain present throughout life could lead to sustained and damaging activation of the amyloid-based immune response," says one of the team, Robert Moir from MIND.

 

"A key insight is that it's not direct killing of brain cells by herpes that causes Alzheimer's, rather it's the immune response to the virus that leads to brain-damaging neuroinflammation."

It's important to note that so far these links have only been shown in mice and lab tests. And there are many other variables involved than just herpes – like the misfolded tau proteins that join forces with the amyloid beta plaques to cause havoc in the brain.

With that in mind, it's certainly not time to say a cold sore virus or something like it is the sole cause of Alzheimer's. What the study does show, however, is that it might play a part with other factors, including a person's genetic make-up.

We might even be looking at different root causes triggering similar biological mechanisms that lead to Alzheimer's in different people.

Tanzi, Moir, and their colleagues are continuing their research, which includes analysing the microbiome of the brain and whether its disruption could also be involved. The ultimate aim is finding a treatment for what's currently an untreatable disease.

That's still some way off, but for now the virus-to-Alzheimer's link is looking stronger than it's ever been – a link often dismissed in the past.

"I think we've gotten past the point where this idea is ridiculed," Tanzi told Ed Cara at Gizmodo.

The research has been published in Neuron.

 

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