Letter to the Editor

Ill-Fated Amyloid-� VaccineThe premature suspension of the amyloid-� vaccine

for the treatment of Alzheimer disease (AD), while disap-pointing, is not surprising. Amyloid-� serves a key role inredox homeostasis (Nunomura et al., 2001) and its re-moval, by vaccination (or others) strategies, would bepredicted to increase oxidative stress and consequently ledto an inflammatory cascade (Perry et al., 2002). Suchinflammation of the brain lead to the halting of the vaccinetrial and should also cause all in the field to pause forthought before pursing other amyloid-�-based therapeu-tics which will also likely exacerbate the disease process(Smith et al., 2000; Joseph et al., 2001).

Mark A. Smith*Craig S. AtwoodJames A. JosephGeorge PerryInstitute of Pathology,Case Western Reserve University,2085 Adelbert Road, Cleveland, Ohio

REFERENCES

Joseph J, Shukitt-Hale B, Denisova NA, Martin A, Perry G, Smith MA.2001. Copernicus revisted: amyloid beta in Alzheimer’s disease. Neuro-biol Aging 22:131–146.

Nunomura A, Perry G, Aliev G, Hirai K, Takeda A, Balraj EK, Jones PK,Ghanbari H, Wataya T, Shimohama S, Chiba S, Atwood CS, PetersenRB, Smith MA. 2001. Oxidative damage is the earliest event in Alzhei-mer disease. J Neuropathol Exp Neurol 60:759–767.

Perry G, Nunomura A, Raina AK, Smith MA. 2000. Amyloid-� junkies.Lancet 355:757.

Smith MA, Joseph JA, Perry G. 2000. Arson: tracking the culprit inAlzheimer’s disease. Ann N Y Acad Sci 924:35–38.

*Correspondence to: Mark A. Smith, Institute of Pathology, Case WesternReserve University, 2085 Adelbert Road, Cleveland, OH 44106.E-mail: mas21@po.cwru.edu

Published online 11 June 2002 in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/jnr.10316

Journal of Neuroscience Research 69:285 (2002)

© 2002 Wiley-Liss, Inc.