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In recent studies of transgenic models of Alzheimer's disease (AD), it has been reported that antibodies to aged beta amyloid peptide 1–42 (Aβ₁₋₄₂) solutions (mixtures of Aβ monomers, oligomers and amyloid fibrils) cause conspicuous reduction of amyloid plaques and neurological improvement. In some cases, however, neurological improvement has been independent of obvious plaque reduction, and it has been suggested that immunization might neutralize soluble, non‐fibrillar forms of Aβ. It is now known that Aβ toxicity resides not only in fibrils, but also in soluble protofibrils and oligomers. The current study has investigated the immune response to low doses of Aβ₁₋₄₂ oligomers and the characteristics of the antibodies they induce. Rabbits that were injected with Aβ₁₋₄₂ solutions containing only monomers and oligomers produced antibodies that preferentially bound to assembled forms of Aβ in …