Abstract: Recent progress in the treatment of Alzheimer’s disease (AD) using antibodies against amyloid sustains amyloid generation as a key process in AD. Amyloid formation starts with two amyloid-beta (Aβ) molecules interacting (dimer formation) followed by an accelerating build-up of so-called protofibrils, which turn into fibrils, which accumulate in the characteristic plaques. To interfere with the process at the root we used molecular modeling to define the surfaces of interaction in dimer formation. In a series of small molecules, we identified candidates that changed the course of interactions and generated aggregates with other macrostructures and reduced toxicity. We have introduced the term “decoys” to identify these molecules.