Study finds copper-based drug reduces toxic Alzheimer's proteins

A team of researchers in Australia has found that a drug which delivers copper to the brain can significantly reduce toxic Alzheimer’s proteins and improve long-term spatial memory in laboratory experiments. The study shows that Cu(ATSM), a copper compound capable of penetrating the brain and helping clear toxic proteins, can repair a vital waste-removal pump at the blood-brain barrier, opening a new avenue for treating neurovascular dysfunction caused by Alzheimer’s and other forms of dementia, which are a leading cause of death in Australia, according to a statement from Monash University released on Monday. In Alzheimer’s disease, this system, driven by the P-glycoprotein (P-gp) pump, becomes impaired, allowing toxic amyloid-beta proteins to accumulate in the brain, the researchers said. The findings, published in ACS Chemical Neuroscience, provide a strong foundation for exploring biometal therapies such as Cu(ATSM) to combat vascular dysfunction and memory loss in Alzheimer’s disease. Lead author Jae Pyun, a lecturer at the Monash Institute of Pharmaceutical Sciences (MIPS), said the treatment successfully engaged the brain’s blood vessels to lower levels of toxic proteins, resulting in improved behavioural outcomes. The study demonstrated that Cu(ATSM) increased P-gp levels by 24.1 per cent in an Alzheimer’s model, effectively linking blood-brain barrier repair with toxic protein reduction and enhanced cognitive function, Pyun said. By improving the pump’s function, the brain can finally clear trapped waste. Over 56 days, the treatment reduced toxic amyloid-beta by approximately 42 per cent and improved spatial learning by nearly 44 per cent, he added. Senior author Professor Joseph Nicolazzo from MIPS said Cu(ATSM), a copper compound with anti-inflammatory and neuroprotective properties, has been safely tested in clinical trials for Parkinson’s disease and ALS, potentially accelerating its path into human studies for Alzheimer’s disease.