WASHINGTON (AP) — An experimental drug might help slow early Alzheimer’s disease in a markedly different way than today’s treatments — by lowering levels of a brain protein called tau, researchers reported Tuesday.

Tau is one part of a toxic duo fueling Alzheimer’s but prior attempts to develop drugs that can target the protein have failed. Two Alzheimer’s drugs, lecanemab and donanemab, try to clear buildup of the better-known amyloid protein and can modestly slow cognitive decline.

The new findings suggest Biogen’s diranersen did more than lower tau levels. The study of about 400 people found signs that it also slowed cognitive decline, in one small subset enough to be comparable to amyloid therapy, according to results presented at the Alzheimer’s Association International Conference in London. Biogen is planning a larger study to try to prove the drug’s benefit.

Researchers at Weill Cornell Medicine and Birkbeck, University of London, have identified a site where a commonly used anesthetic binds to sodium ion channels, revealing a molecular mechanism that may explain how these drugs dampen communication between neurons. Ion channels are proteins that regulate the flow of charged particles across cell membranes, enabling neurons to generate electrical signals. By reducing this signaling, inhaled anesthetics help suppress brain activity, producing unconsciousness and immobility during surgery.

The findings, published June 19 in Nature Communications, shed light on a longstanding mystery: For 175 years, doctors have safely used inhaled anesthetics to render patients unconscious, but didn’t fully understand how these drugs work.

“Sodium channels are critical for communication between neurons in the brain, and anesthesia breaks down that communication,” said Dr. Hugh Hemmings, senior associate dean for research and chair of the Department of Anesthesiology at Weill Cornell, who co-led the research. “So, there’s good reason to believe that the unconsciousness produced by volatile anesthetics is related to their effects on sodium channels.”

The researchers then tested BA-101 together with temozolomide and found that the combination was more effective than either treatment alone. In experiments using mouse models, the combined therapy significantly reduced tumor growth, suggesting that targeting the cancer cells’ resistance mechanism could make existing chemotherapy more powerful.

“Temozolomide resistance remains one of the biggest obstacles in treating glioblastoma,” said Amal. “Our findings suggest that targeting nitrosative stress can restore the tumor’s sensitivity to treatment. While additional studies are needed before this approach can reach patients, these results open an exciting new direction for developing more effective therapies against one of the deadliest cancers.”

The researchers said their findings could point to a new approach in cancer treatment: instead of replacing existing drugs, future therapies could focus on blocking the mechanisms that allow tumors to resist them. If further studies confirm the findings, disabling these survival pathways could allow treatments that have become less effective to regain their ability to attack cancer cells.