Copper compound restores memory in Alzheimer’s lab tests

A copper-based drug has shown potential to reduce toxic protein buildup and improve memory in laboratory models of Alzheimer’s disease. Researchers at Monash University found that the compound Cu(ATSM) enhanced the brain’s waste-clearing mechanisms. The results were published in ACS Chemical Neuroscience.

The study demonstrated that Cu(ATSM) increased levels of P-glycoprotein pumps in the blood-brain barrier by 24.1 percent. This led to a 42 percent reduction in amyloid-beta proteins over 56 days.

Spatial learning improved by nearly 44 percent in treated models. Lead author Dr. Jae Pyun noted that the treatment links repair of the blood-brain barrier to lower toxic proteins and better cognitive function.

Senior author Professor Joseph Nicolazzo highlighted that the drug has already undergone human safety testing for Parkinson’s disease and ALS. This could allow faster progression to trials in Alzheimer’s patients.

The findings support further research into biometal-based approaches for treating neurovascular issues linked to dementia.

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Oregon State scientists tracking copper-driven amyloid-beta clumping in real time using fluorescence anisotropy, with chelators reversing aggregation, in a high-tech lab.
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Oregon State researchers track copper-driven amyloid clumping in real time, testing a copper-selective chelator

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Oregon State University scientists report they have monitored, second by second, how copper ions promote aggregation of amyloid-beta—an Alzheimer’s-associated protein—and how different metal-binding molecules can disrupt or reverse that clumping, using a fluorescence anisotropy approach described in a study published in ACS Omega.

Researchers from the Institute for Bioengineering of Catalonia and collaborating institutions report that engineered “supramolecular” nanoparticles restored aspects of blood-brain barrier function in Alzheimer’s-model mice, rapidly lowering brain amyloid-β and producing improvements on behavioral and memory tests.

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Researchers at Cold Spring Harbor Laboratory have found that blocking the protein PTP1B improves memory and boosts plaque clearance in mouse models of Alzheimer's disease. The discovery links the protein to brain immune function and metabolic risks like diabetes and obesity. The team aims to develop inhibitors for potential human treatments.

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