A copper-based drug could offer a new route to tackling Alzheimer’s disease, after researchers found it reduced toxic proteins in the brain while improving memory in laboratory studies.
How Toxic Proteins Build Up in Alzheimer’sAlzheimer’s develops in part due to the build-up of amyloid-beta in the brain.
Advertisement AdvertisementHowever, this system becomes less efficient over time in Alzheimer’s patients, allowing harmful proteins to accumulate.
When these pumps lose function, the brain’s ability to clear toxic material is significantly reduced.
One theory is that Cu(ATSM) may also boost the activity of microglia—immune cells that help break down toxic proteins.
A copper-based drug could offer a new route to tackling Alzheimer’s disease, after researchers found it reduced toxic proteins in the brain while improving memory in laboratory studies.
Scientists at Monash University reported that the compound, known as Cu(ATSM), not only lowered levels of amyloid-beta—a protein strongly linked to Alzheimer’s—but also improved long-term spatial memory.
Their findings, published in ACS Chemical Neuroscience, point to a treatment that targets the brain’s waste-removal system, a process known to break down in people with the disease.
A stock image shows a doctor’s hand pointing at a brain scan image on a computer screen.
How Toxic Proteins Build Up in Alzheimer’s
Alzheimer’s develops in part due to the build-up of amyloid-beta in the brain. Under normal conditions, these proteins are cleared away through the blood-brain barrier, a protective layer that controls what enters and leaves the brain.
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However, this system becomes less efficient over time in Alzheimer’s patients, allowing harmful proteins to accumulate.
A central role in this process is played by P-glycoprotein (P-gp) pumps—transport proteins that help move waste products out of the brain and into the bloodstream. When these pumps lose function, the brain’s ability to clear toxic material is significantly reduced.
What the Study Found About Cu(ATSM)
The new study shows that Cu(ATSM) may help restore this system by increasing the number and activity of these pumps. Lead author Dr. Jae Pyun explained that the treatment works by improving the function of the brain’s blood vessels, leading to both lower toxic protein levels and better cognitive performance.
“This is the first study to show that Cu(ATSM) can increase the abundance of P-gp clearance pumps in an Alzheimer’s model, by 24.1 percent, effectively linking the repair of the blood-brain barrier to a reduction in toxic proteins and improved cognitive function,” Dr. Pyun said.
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The team found that restoring this waste-removal pathway had a measurable effect. “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.”
The results suggest that repairing the blood-brain barrier could be key to slowing or reversing some of the damage seen in Alzheimer’s disease.
A Drug Already Tested in Other Conditions
Senior author Professor Joseph Nicolazzo said the drug could move toward human trials more quickly than some other experimental treatments. That is because Cu(ATSM) has already been tested for safety in other neurological conditions.
“Cu(ATSM) is a copper compound with anti-inflammatory and neuroprotective properties that has already progressed to clinical testing for conditions like Parkinson’s and ALS,” Nicolazzo said.
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He added that the reduction of amyloid in the brain is a meaningful target for improving symptoms. “Because reducing amyloid burden is clinically proven to improve functional outcomes, these preclinical results strongly support the rationale for testing this drug in early symptomatic Alzheimer’s disease.”
What Remains Unknown
While the findings are promising, researchers are still working to understand exactly how amyloid-beta leaves the brain once the barrier is restored. One theory is that Cu(ATSM) may also boost the activity of microglia—immune cells that help break down toxic proteins.
Dr. Dayan Goodenowe, a Ph.D. neuroscientist who is not directly connected to this specific study, told Newsweek that targeting the blood-brain barrier and waste-clearance systems is a promising area because Alzheimer’s is not just a plaque-storage problem.
“Alzheimer’s involves the biological environment of the aging brain and including membrane biology, inflammation, vascular function, lipid metabolism and cellular resilience… All of those components…” he said. “So any SINGLE mechanism still has to be validated before we know whether it produces meaningful clinical benefit.”
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According to Goodenowe, the biology suggests that amyloid may be influenced by the broader lipid environment of the brain.
“The key question is not simply whether amyloid changes, but whether the intervention improves cognition, function and outcomes in humans,” he said. “The research must move from mechanism and preclinical work to human safety, dose, efficacy and ultimately FDA governed validation.”
What This Could Mean for Future Treatment
Further studies will explore these pathways in more detail. For now, the results highlight the potential of therapies that target both blood vessel function and protein clearance mechanisms in the brain.
With dementia rates rising and the need for effective treatments becoming more urgent, the study offers early evidence that repairing the brain’s natural cleaning system could play a crucial role in future Alzheimer’s therapies.
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