Increasing evidence suggests that amyloid peptides associated with a variety of
degenerative diseases induce neurotoxicity in their intermediate oligomeric state, rather
than as monomers or fibrils. To test this hypothesis and investigate the possible involvement
of Ca 2+ signaling disruptions in amyloid-induced cytotoxicity, we made homogeneous
preparations of disease-related amyloids (Aβ, prion, islet amyloid polypeptide,
polyglutamine, and lysozyme) in various aggregation states and tested their actions on fluo …