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Arch Neurol. 2003;60:1678-1679.

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

THE AMYLOID cascade hypothesis states that the dementia of Alzheimer disease (AD) is caused in part by the toxic accumulation of -amyloid (A) in extracellular amyloid-containing neuritic plaques and as accumulations of neuronal cytoplasmic A oligomers.¹ On the basis of this hypothesis, blocking the formation of A from the amyloid precursor protein by inhibiting the enzymes -secretase and -secretase has been a therapeutic strategy.¹ Immunization with A, which effectively removed A or prevented the development of A plaque formation in transgenic mice carrying the human V717 F transgene, has been another clinical therapeutic approach. Vaccination with A in patients resulted in clinical meningoencephalitis, so clinical trials had to be suspended.² Innovative alternative strategies for reducing A synthesis and accumulation are needed; in this issue of the ARCHIVES, Ritchie and colleagues³ present a novel strategy for reducing A neurotoxcitity by attenuation of A–metal ion interactions. As they point . . . [Full Text of this Article]

Roger N. Rosenberg, MD, Editor
Archives of Neurology
Department of Neurology
University of Texas Southwestern Medical Center
5323 Harry Hines Blvd
Dallas, TX 75390-9108
(e-mail: archneurol@jama-archives.org)

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