The Startling Link Between Alzheimer’s And Our Ancient Immune System

Alzheimer’s Disease was named and identified in the early 20th Century, but it wasn’t until the ’70s and ’80s that heavy research actually began. Since then, it’s become widely accepted that a build-up of beta-amyloid and tau proteins in the brain leads to the disease, and that the beta-amyloid protein itself is a waste product of no real use.

But for the past several years, a pair of scientists, Rudolph Tanzi and Robert Moir, have been researching the amyloid protein and conducting experiments. Their work has led them to propose a startling theory: beta-amyloid is actually an antimicrobial protein that helps protect the brain — when it appears in normal levels.

Photo: Adobe Stock/Juan Gärtner
Photo: Adobe Stock/Juan Gärtner

As far back as 2007, Tanzi and Moir separately discovered that there was a connection between Alzheimer’s and mankind’s innate immunity. After discussing their findings, the two neuroscientists teamed up to study it further.

“Turns out, our most ancient immune system, before we had adaptive immunity, had little baby proteins, antimicrobial peptides,” Rudolph Tanzi told the Daily Beast. “And when they saw bacteria or a virus or a fungus, they would stick to it and clump it up into a ball and the peptide would grow into a spiral like spaghetti and trap it like a fly trapping a seed, and that is one of the most classic ways that our primitive innate immune system protects us.”

Antimicrobial peptides are common to all forms of life and are part of our ancient immune system. Without them to protect the brain against foreign invaders, we’d die in a few hours.

One of the ancient peptides Moir found during the course of his research is called LL-37 — and it is molecularly similar to the amyloid beta protein.

The similarity got the men thinking. They hypothesized that beta-amyloid functioned in the brain like a pearl in an oyster — as a system of self defense and “a way for our body to trap and permanently sequester these invading pathogens,” Moir told NPR.

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Photo: Adobe Stock/Andrey Burmakin
Photo: Adobe Stock/Andrey Burmakin

So Tanzi and Moir began doing experiments. First, they proved that the amyloid protein could kill viruses in a test tube environment. They put Alzheimer’s genes and a microbe in a petri dish, and found that amyloid plaques grew overnight, running contrary to the theory that they take years to build up.

In later studies on mice, they found that amyloid built up in mice within 48 hours. They also proved it could kill viruses in worms.

This rapid development of amyloid proteins astonished both Tanzi and Moir, and the scientific community. And while their findings weren’t initially well-received — since it was commonly accepted that amyloid proteins were not helpful in any way and also took years to develop — eventually, other researchers began to see that Moir and Tanzi might be on to something.

Instead of focusing on the amyloid build-up itself, shouldn’t our focus be on the microbes that cause that build-up?

Photo: Adobe Stock/ugreen
Photo: Adobe Stock/ugreen

Their theory could help explain why Alzheimer’s typically develops late in life. Our immune system and blood-brain barrier start to fail as we age, and that weakening of our defenses could allow infections to slip in and increase the amount of beta-amyloid in our brains. Then, like dominoes, that could trigger the development of tangles and inflammation.

It’s also possible that some people’s immune systems get confused as they age, and begin attacking healthy cells, like what occurs in lupus or multiple sclerosis.

Tanzi and Moir have partnered with Cure Alzheimer’s Fund and Open Philanthropy to continue their research, focusing on identifying all the microbes found in an aging brain and looking at autopsies of Alzheimer’s brains.

Photo: Facebook/Cure Alzheimer's Fund
Photo: Facebook/Cure Alzheimer’s Fund
Robert Moir & Rudolph Tanzi

The ultimate goal is to find effective treatment options for Alzheimer’s, and Tanzi and Moir are hopeful that their research will lead to new treatments, and a way to stop or prevent Alzheimer’s years before symptoms appear.

Finding a way to target the specific microbes that prompt the overproduction of amyloid (rather than the amyloid itself) is one course of action, since attacking the amyloid after they’ve formed doesn’t stop cognitive decline. Another option could be developing a test for young adults. If doctors were able to see and track what brains were more susceptible to this type of amyloid build-up response, they could focus on preventative measures sooner.

Their research challenges the theory that Alzheimer’s comes down to plaques and tangles. “Even though we really concentrate on these plaques and tangles in Alzheimer’s disease, it looks like it’s the brain’s immune system — the very primitive immune system of the brain — that’s gone awry,” Tanzi told NPR, “and the plaques and tangles are a part of that system.”

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