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Copper drug cuts amyloid and boosts memory in mouse study

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Monash University researchers report that copper‑delivery compound Cu(ATSM) cuts amyloid‑beta and boosts spatial memory in mouse Alzheimer model. The drug restores P‑glycoprotein pumps at the blood‑brain barrier, allowing waste clearance. Lead author Dr Jae Pyun says treatment raised pump abundance by 24.1% and lowered toxic protein levels over a 56‑day regimen, mice showed significant behavioral improvement compared to controls in tests.

Senior author Prof Joseph Nicolazzo notes Cu(ATSM) already cleared safety tests for Parkinson’s and ALS, shortening path to clinical trials for Alzheimer’s. Over the 56‑day study the compound reduced amyloid burden by 42% and enhanced spatial learning by roughly 44%. Researchers also suspect copper may activate microglia to degrade plaques, though exact clearance routes remain unclear.

Australia now lists dementia as its leading cause of death, heightening urgency for disease‑modifying therapies. The Monash team’s findings suggest biometal delivery can repair neurovascular dysfunction, a root cause of protein accumulation. If human trials confirm these effects, Cu(ATSM) could become the first drug to improve both barrier integrity and cognition in early Alzheimer patients.