Scientists believe they have identified a key mechanism behind the spread of Alzheimer’s disease through the brain, a discovery that could open the door to new treatments aimed at slowing the condition rather than simply clearing away toxic proteins after damage is done.

Researchers at the University of Utah Health found that a brain protein called Arc, which normally helps neurons communicate with one another, may be inadvertently helping the disease spread. The protein appears to carry toxic Tau—a hallmark of Alzheimer’s—out of damaged brain cells and into healthy ones.

Dr. Christopher U. Missling, president of Anavex Life Sciences, a biotechnology company focused on central nervous system disorders including Alzheimer’s, told Newsweek the breakthrough findings reframe how scientists think about the disease.

“For decades, research has focused on the toxic buildup of Tau inside neurons; this study reframes the problem by showing how Tau may exploit the brain’s own communication machinery, specifically the Arc protein and its extracellular vesicle system, to spread between cells,” Missling said.

He added that the discovery “underscores how normal synaptic signaling proteins can become hijacked in disease, blurring the line between physiological and pathological communication,” and that targeting this transport system might one day help slow or contain Alzheimer’s spread rather than trying to eliminate Tau entirely.

How Tau Hitches a Ride

Alzheimer’s disease is driven by the buildup of Tau, a protein that clumps into sticky tangles inside neurons, disrupting their internal machinery and eventually killing them. As Tau spreads to new regions of the brain, memory loss and cognitive decline worsen.

To understand how this spread happens, researchers compared mice with Alzheimer’s-like disease to mice that also lacked the Arc protein. They found Arc plays an essential role in moving Tau between cells.

Normally, Arc packages itself into tiny structures called extracellular vesicles, which shuttle between neurons carrying important cellular signals. But the study found that toxic Tau can hitch a ride inside these same vesicles, using Arc to travel from a diseased neuron into a healthy one, where it can trigger new tangles to form.

When Arc was removed from the mice, the vesicles carried far less Tau, and the disease no longer spread effectively between neurons.

A Protective Role Complicates the Picture

The results were not entirely straightforward. Arc also appears to do the positive job of helping neurons survive longer in the early stages of disease by allowing them to expel excess toxic Tau.

That finding suggests simply blocking Arc altogether may not be the answer. Instead, researchers believe future treatments should focus on preventing the Tau-carrying vesicles from entering healthy neurons, while still allowing damaged cells to expel their toxic waste.

A Potential New Target for Alzheimer’s Therapies

The team also detected extracellular vesicles containing both Arc and Tau in human brain tissue, suggesting the same process could be at work in people. Researchers caution that significant further study, especially on humans, is needed before the findings could lead to any treatment, but they say the discovery offers a promising new target for future therapies aimed at slowing, rather than eliminating, the disease’s spread through the brain by intercepting Tau containing extracellular vesicles after they leave diseased neurons, before they reach healthy ones. 

The study was published in Cell on June 29.

Contact Newsweek editors on this story: Kara Dolman and Emma Lee-Sang.

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