ALZHEIMER DISEASE (AD) may result from the cortical accumulation of β-amyloid (Aβ). Several strategies to inhibit Aβ production and/or accumulation have been explored in experimental models of AD and are now being translated into double-blinded clinical trials.^1,2 We have developed a strategy of targeting Aβ through metal-protein–attenuating compounds (MPAC), which promote the solubilization (and clearance) of Aβ and inhibit redox-active copper ion (Cu²⁺)–Aβ interactions that generate neurotoxic hydrogen peroxide.^3,4 One such MPAC lead compound, iodochlorhydroxyquin (an anti-infective agent also known as clioquinol) induces a rapid decrease in brain Aβ deposition in a mouse model of AD.⁵ Clioquinol also inhibits Aβ toxicity in neuronal cell cultures, ⁶ possibly acting through an additional mechanism of preventing Aβ-lipid interactions.⁷