Neuronal Cyclooxygenase 2 Expression in the Hippocampal Formation as a Function of the Clinical Progression of Alzheimer Disease

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Abstract
A LARGE NUMBER of epidemiologic studies have indicated that the use of nonsteroidal anti-inflammatory drugs (NSAIDs) may prevent or delay the clinical features of Alzheimer disease (AD).1-3 The pharmacologic activity of NSAIDs is generally attributed to inhibition of cyclooxygenase (COX), a rate-limiting enzyme in the production of prostaglandins. Two distinct COX isoforms have been characterized: a constitutive form, COX-1, and a mitogen-inducible form, COX-2.4 Characterization of COX expression in the brain may be important to understanding the potential therapeutic effect of NSAIDs and to devising optimal treatment regimens.