In transgenic mouse models of Alzheimer's disease (AD), immunization with beta-amyloid peptide A beta 1-42 slows or reverses disease progression and provides neuronal protection and improvement in memory tasks. Development of a safe and effective immunization strategy for therapeutic use requires an understanding of the immune system components involved in these responses. A key discovery has been that reduction of AD-like neuropathologies can be obtained with passive administration of antibodies, and that a T cell response against Abeta is not required. Several mechanisms have been suggested to be involved in efficacy, including antibody Fc-mediated and Fc-independent events; these mechanisms are reviewed here.
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