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Arch Neurol. 2004;61:1832.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Accumulation of amyloid- (A_40 – 42) peptides that are generated by proteolytic processing of amyloid precursor protein is widely considered to play a major role in the neurodegeneration of Alzheimer disease (AD), and the amelioration of amyloid burden is a hot target for the treatment of AD. Immunization by A₄₂ peptide has been demonstrated to lead to reduction of A burden accompanied by improved cognitive performance in a mouse transgenic model of AD.¹ This approach of A₄₂ peptide immunization has been applied in a clinical trial of patients with AD. About 300 patients with AD received multiple doses of the A₄₂ peptide with the adjuvant QS21. Although patients with higher antibody titer (20%) seemed to show a slowing of the cognitive decline, the program was discontinued owing to the fact that about 6% of treated patients developed autoimmune meningoencephalitis.^2-4 This experience suggests that A₄₂ peptide immunization is potentially an effective treatment . . . [Full Text of this Article]

AUTHOR INFORMATION

Shoji Tsuji, MD, PhD

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ABSTRACT | FULL TEXT