Researchers identified a brain protein that appears to help the disease spread between neurons, opening a potential new avenue for future treatments.

Scientists may have uncovered a new clue to how Alzheimer’s disease spreads through the brain, a discovery that could one day lead to new treatments.

Researchers have long known that a toxic protein called tau spreads across the brain in Alzheimer’s patients, where it kills brain cells and drives cognitive decline. However, in a new study published in the peer-reviewed journal Cell, investigators at the University of Utah found that Arc, a brain protein that helps neurons communicate, also helps package and transmit tau across the brain cells. 

“I had a hunch Arc may be involved, but wasn’t expecting our results to be so clear,” Jason Shepherd, a professor in the University of Utah’s department of neurobiology and lead researcher in the study, told Inc. “When my student [Mitali Tyagi, a co-author of the study] first found that tau transmission was almost gone in neurons that lacked Arc, I was surprised and excited.”

Arc’s role in mice

To investigate how Arc operates, Shepherd’s team compared brain activity in mice with and without the protein. Ten weeks after injecting the mice with tau, they found that neuron-to-neuron tau transmission was significantly reduced in mice lacking Arc, suggesting the protein plays a critical role in helping tau spread, according to the study.

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The finding identifies a potential new target for slowing Alzheimer’s progression.

“Many neurodegenerative diseases have a similar origin: toxic misfolded proteins that kill neurons,” Shepherd says. “Over time, these toxic proteins spread across the brain, but this process is slow. If we could stop this spread early in the disease, we could potentially completely stop the disease from getting worse.”

Arc is still essential to brain health

However, this doesn’t mean eliminating Arc is the answer.

Although Arc appears to facilitate the spread of toxic tau, it also plays a vital role in learning and memory. Any future Alzheimer’s treatment targeting Arc would need to preserve its normal function while preventing it from transporting tau, Shepherd says.

More research is also needed before the findings can be translated to people.

“Most of our studies have been done in mice, so even though all these proteins are highly conserved in humans, we still need to know if similar processes are causally involved in the transmission of tau in human neurons,” Shepherd says. “Our next studies aim to test this.”

This post originally appeared at inc.com.

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