New Alzheimer’s research uncovers a possible clue to the disease

Imagine someone showing up at work, taking over your job and leaving you with nothing productive to do.

Something similar may happen inside brain cells as Alzheimer’s disease develops, according to a recent study.

Researchers found that a protein called amyloid beta can compete with another protein, tau, for the same location inside brain cells. If enough amyloid beta builds up, it may push tau aside, potentially setting off a cascade of changes associated with Alzheimer’s.

“The study suggests a unifying connection between the two main proteins, amyloid beta and tau, involved with Alzheimer’s disease,” says Dr. Darren Gitelman, a behavioral neurologist and senior medical director of the Advocate Memory Center. “Understanding the dysfunction of these proteins early in the disease process could give researchers important clues about what drives Alzheimer’s and where there may be opportunities to intervene.”

What normally happens inside a brain cell?

To understand what the researchers found, it helps to know what tau usually does.

Brain cells contain tiny tubes called microtubules that act like an internal scaffolding and transportation system that helps move materials the cells need to survive and communicate. Tau proteins attach to the microtubules and help keep them stable.

The researchers noticed that the part of tau that attaches to microtubules looked similar in size and structure to amyloid beta. That led them to wonder: Could amyloid beta attach there too?

What did the researchers discover?

Researchers tracked amyloid beta and found that the protein attached to microtubules. They also discovered that amyloid beta and tau bind to the microtubules with about the same strength.

That means if enough amyloid beta accumulates inside a brain cell, it could compete for the same spots and take over tau’s job.

How could that contribute to Alzheimer’s?

Researchers theorized that the competition between the two proteins could create problems in two ways.

Without tau binding to stabilize the microtubules, the brain cell’s transportation system could begin to break down. Meanwhile, displaced tau could build up in other parts of the cell, potentially causing further damage.

The theory could help explain how two proteins closely associated with Alzheimer’s may be connected.

“This study gives us a possible explanation for how changes involving these two proteins may work together to damage brain cells,” Dr. Gitelman says. “But it’s still a theory that researchers will need to test further.”

Could the discovery lead to new treatments?

If further research supports the theory, the findings could give scientists new ideas about treating Alzheimer’s.

In addition to studying ways to address buildups of amyloid beta and tau, researchers could explore how to prevent amyloid beta from interfering with microtubules or help brain cells clear the protein before it causes problems.

“The more we understand about what drives these changes in the brain, the better our opportunities may be to treat Alzheimer’s,” Dr. Gitelman says.

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