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Editorial
October 2005

Immunotherapy for Alzheimer DiseaseThe Promise and the Problem

Arch Neurol. 2005;62(10):1506-1507. doi:10.1001/archneur.62.10.1506

Immunization therapy for Alzheimer disease (AD) entered the realm of possibility with the startling publication in 1999 by Schenk et al1 of the successful immunization of transgenic mice carrying a human mutant gene for the amyloid precursor protein, causal of early onset AD,1,2 that resulted in a striking reduction in brain amyloid burden with reduced gliosis and dystrophic neurites in immunized β-amyloid(1-42) (Aβ[1-42])–transgenic mice. As a result of the highly positive reduction of amyloid burden in Aβ(1-42)-immunized transgenic mice with improved behavior and memory,3,4 a phase II double-blind, placebo-controlled, multicenter study was conducted to evaluate safety, tolerability, and pilot efficacy of AN1792 (Aβ[1-42]) administered with AS21 adjuvant in 372 patients with mild to moderate AD. Unfortunately, this study had to be stopped owing to the development of meningoencephalitis associated with AN1792 immunization in 18 of 300 immunized patients. By the time the study was discontinued, 24 patients had received 3 immunizations, and 274 patients had received 2 immunizations. There was evidence of some benefit to patients who received immunotherapy immunizations, with improvement in some neuropsychological test scores and in enhanced quality-of-life scores.58

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