Abstract
Amyloid-β (Aβ) accumulation in the brain is a cardinal event in Alzheimer's disease (AD), but the structural basis of Aβ-elicited neurotoxicity is unknown. In a recent paper, Ciudad et al. elucidate the first atomic structures of Aβ oligomers, which reveal how they form lipid-stabilized pores that might disrupt neuronal membranes and ion homeostasis.