Study finds copper drug restores memory, cuts toxic Alzheimer's proteins-Xinhua

Study finds copper drug restores memory, cuts toxic Alzheimer's proteins

Source: Xinhua

Editor: huaxia

2026-06-15 14:56:30

MELBOURNE, June 15 (Xinhua) -- Researchers in Australia have found that a drug which delivers copper to the brain significantly reduces toxic Alzheimer's proteins and improves long-term spatial memory in laboratory experiments.

The study shows Cu(ATSM), a brain-penetrating copper compound that helps clear toxic proteins, repairs a vital waste-clearing pump at the blood-brain barrier, opening a new avenue for treating neurovascular dysfunction caused by Alzheimer's and other dementias, Australia's leading cause of death, according to a statement from Australia's Monash University released on Monday.

In Alzheimer's disease, this system, driven by P-glycoprotein (P-gp) pumps, becomes impaired, allowing toxic amyloid-beta proteins to build up in the brain, researchers said.

The findings, published in ACS Chemical Neuroscience, establish a strong foundation for exploring biometal therapies such as Cu(ATSM) to combat blood vessel dysfunction and memory loss in Alzheimer's disease.

Lead author Jae Pyun, lecturer at Monash Institute of Pharmaceutical Sciences (MIPS), said the treatment successfully engages the brain's blood vessels to lower toxic protein levels, resulting in behavioral benefits.

The study showed that Cu(ATSM) increased P-gp levels by 24.1 percent in an Alzheimer's model, "effectively linking the repair of the blood-brain barrier to a reduction in toxic proteins and improved cognitive function," Pyun said.

"By improving the pumps, the brain can finally clear out the trapped waste. Over 56 days, the treatment reduced toxic amyloid-beta by 42 percent and improved spatial learning by nearly 44 percent," he added.

Senior author Professor Joseph Nicolazzo at MIPS said Cu(ATSM), a copper compound with anti-inflammatory and neuroprotective properties, has already been tested safely in clinical trials for Parkinson's and ALS, potentially speeding its path to Alzheimer's human studies.