The pathology of Alzheimer's disease shows a significant correlation between β-amyloid peptide conformation and the clinical severity of dementia. For many years efforts have been focused on the development of inhibitors of β-amyloid formation and its related neurotoxic effects. A new concept has been developed which shows that site-directed antibodies may modulate formation of β-amyloid. The performance of anti-β-amyloid antibodies in transgenic mice models of Alzheimer's disease showed that they are delivered to the central nervous system, preventing in vivo formation of β-amyloid. Moreover, those antibodies dissolve β-amyloid plaques and protect the mice from learning and age-related memory deficits. Experimental active immunization with β-amyloid (1-42) in humans was stopped in phase II of their clinical trials. However, several new preparations, able to provide antibodies against β-amyloid by either active or passive routes, have been formulated and have reached clinical testing. The data presented support the hypothesis that β-amyloid peptide plays a central role in Alzheimer's disease, and antibodies which modulate β-amyloid conformation may lead to immunotherapy of the disease.