An analysis of the brain of a deceased Alzheimer’s disease (AD) clinical trial participant found that regions where an anti-amyloid therapy successfully cleared amyloid plaques showed little to no evidence of tau tangles, a hallmark of AD closely linked to neurodegeneration and cognitive decline. In contrast, neighboring areas where amyloid remained showed substantially more tau pathology and signs of ongoing brain damage.

The findings provide rare human evidence that clearing amyloid plaques may have long-term effects on the biological processes that drive AD. The study also suggests that removing amyloid early and extensively may slow the progression of the disease by limiting the accumulation of tau and subsequent neurodegeneration, according to findings presented July 13 at the 2026 Alzheimer’s Association International Conference by researchers from the Perelman School of Medicine at the University of Pennsylvania. The report was also concurrently published in JAMA.

“Seeing both disease patterns side-by-side in the same brain gave us a rare opportunity to understand how amyloid removal affects other proteins that contribute to Alzheimer’s disease,” said co-senior author David Wolk, MD, co-director of the Penn Memory Center and director of the Penn Alzheimer’s Disease Research Center. “The findings provide some of the clearest human evidence to date that anti-amyloid therapies may limit the accumulation of tau and slow the brain changes that lead to memory loss and cognitive decline.”

GLP-1 drugs show promise for more than weight loss. They also cut substance abuse and are changing how we think about the brain’s reward system.

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.”