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2h ago

Copper Compound Restores Brain Clearance Pump and Cuts Alzheimer’s Proteins in Mice

Researchers say prior human safety testing for the drug in Parkinson’s and ALS supports moving toward trials even though how the brain clears the proteins remains unclear.

Using the APP/PS1 mouse model of familial Alzheimer’s disease, Pyun et al. investigated the effect of Cu(ATSM) on brain microvascular abundance and function of P-glycoprotein and the associated effects on exogenous amyloid-beta clearance, brain amyloid burden, and cognitive function. Image credit: Pyun et al., doi: 10.1021/acschemneuro.6c00252.
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Overview

  • The peer‑reviewed study, which was published online May 30, 2026, found that 56 days of Cu(ATSM) treatment produced measurable changes in an APP/PS1 mouse model of Alzheimer’s disease.
  • Cu(ATSM) increased P‑glycoprotein (P‑gp) abundance at the blood–brain barrier by 24.1 percent, a pump that helps move waste from brain to blood.
  • Treated mice showed about a 42 percent drop in brain amyloid‑beta and nearly a 44 percent improvement in long‑term spatial learning compared with untreated mice.
  • Authors say the compound’s prior safety testing in Parkinson’s and ALS could ease the path to human trials, but they stress that human benefit is unproven and the exact clearance routes remain to be mapped.
  • The paper discloses licensed intellectual property and financial ties between some authors and biotech firms, and researchers plan follow‑up studies to trace how cleared proteins exit the brain and the role of microglia.