Schematic depiction of a role for receptor-mediated interaction with pathogenic Aβ assemblies (which could be dimers, multimers, and/or fibrils) in mediating cellular dysfunction early in amyloidoses (left). In contrast, nonspecific neuronal/cellular toxicity (for example, interfering with the integrity of cell membranes) is likely to be an important mechanism of cellular injury at later stages of the disease when there is a higher level of Aβ (right).