en.Wedoany.com Reported - Researchers at Monash University in Australia have discovered in laboratory experiments that a drug delivering copper to the brain can significantly reduce toxic Alzheimer's proteins and improve long-term spatial memory.
The study, published in the journal ACS Chemical Neuroscience, shows that the compound Cu(ATSM) repairs a key waste clearance pump at the blood-brain barrier, opening potential for new therapeutic approaches targeting neurovascular dysfunction.
Alzheimer's disease is driven by the accumulation of toxic proteins called beta-amyloid. Normally, the brain flushes these proteins into the bloodstream via the blood-brain barrier. In Alzheimer's disease, the pump primarily responsible—P-glycoprotein (P-gp)—is significantly weakened, trapping toxic proteins in the brain.
Lead author Dr. Jae Pyun, from the Drug Delivery, Disposition and Dynamics Theme at the Monash Institute of Pharmaceutical Sciences (MIPS), stated that the treatment successfully activated brain blood vessels to reduce toxic protein levels, leading to behavioral benefits. This is the first study to show that Cu(ATSM) can increase the abundance of the P-gp clearance pump by 24.1% in Alzheimer's models, effectively linking blood-brain barrier repair to reduced toxic proteins and improved cognitive function. By improving pump function, the brain can finally clear trapped waste. Over 56 days, the treatment reduced toxic beta-amyloid by 42% and improved spatial learning ability by nearly 44%.
Senior author Professor Joseph Nicolazzo, Director of the MIPS Candidate Drug Optimization Centre, noted that the compound has strong potential for rapid translation into human clinical trials, as it has already been evaluated for safety in other diseases. Cu(ATSM) is a copper compound with anti-inflammatory and neuroprotective properties, already in clinical testing for conditions such as Parkinson's disease and amyotrophic lateral sclerosis (ALS). Given clinical evidence that reducing amyloid burden improves functional outcomes, these preclinical results strongly support the rationale for testing this drug in early symptomatic Alzheimer's disease.
Although the compound reduced amyloid accumulation, researchers are still mapping the specific biological pathways by which these proteins exit the brain. In addition to repairing the blood-brain barrier, researchers suspect that copper therapy may enhance the ability of the brain's own immune cells, called microglia, to engulf and degrade toxic plaques. Future studies will focus on tracking the precise clearance mechanisms to understand how proteins move from the brain into the bloodstream. The current findings lay a solid foundation for exploring biometal therapies like Cu(ATSM) to combat vascular dysfunction and memory loss in Alzheimer's disease.
Alzheimer's disease and other forms of dementia are a growing global health problem, recently surpassing coronary heart disease as the leading cause of death in Australia. With mortality rates continuing to rise and an aging population, finding effective treatments to halt cognitive decline is critical.
The study was led by Dr. Jae Pyun, with collaborators including Pranav Runwal, Oliver Fuller, Casey Egan, Professor Mark Febbraio, Associate Professor Jennifer Short, and Professor Joseph Nicolazzo from the Monash Institute of Pharmaceutical Sciences, as well as Dr. Asif Noor, Celeste Mawal, Professor Paul Donnelly, and Professor Ashley Bush from the University of Melbourne.
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