Central to the amyloid hypothesis of Alzheimer's disease is the primary role of aggregated (3-amyloid (A(beta)) peptide in causing the pathogenesis and loss of cognitive function characteristic of the disease. But the fashionability of A(beta) as a potential therapeutic target suffered a setback last year when Elan/Wyeth-Ayerst's much heralded clinical trial of passive immunization against A(beta) as a treatment for Alzheimer's disease was halted owing to the development of adverse reactions in a subset of patients. At the time, the paucity of information surrounding the reasons for interrupting the trial only increased concern about the validity of the approach, and it was subsequently revealed that 6% of patients had developed a potentially life-threatening asepticmeningoence-phalitis. Although the trial remains suspended, a paper in the 22 May issue of Neuron now reports reduced cognitive decline in a small cohort of enrolled patients that developed a high titre of antibodies to A(beta).
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