New treatment strategies have developed since publication in 1991 of the amyloid hypothesis on the pathogenesis of Alzheimer's disease. In contrast to previous methods, these strategies are not for countering the effects of neuronal loss at the transmitter level. Instead, they are meant to influence the neurodegenerative process itself. They incorporate amyloid precursor protein-splitting proteases (secretase inhibitors), substances for reducing the aggregation of beta-amyloid 42 (Abeta42) and stimulating specific immune reactions against it. Particularly Abeta42 and the clinical research are examined. Ethical and economic questions resulting from successful immunization against Abeta are discussed.