Epidemiological studies indicate that anti-inflammatory drugs, especially the non-steroidal antiinflammatory drugs (NSAIDs), decrease the risk of developing Alzheimers disease (AD). Their beneficial effects may be due to interference of the chronic inflammatory reaction in AD. The best-characterised action of NSAIDs is the inhibition of cyclooxygenase (COX). So far, clinical trials designed to inhibit inflammation or cyclooxygenase activity have failed in the treatment of AD patients. In this review we will focus on the role, expression and regulation of COX-1 and COX-2 in neurodegeneration and AD pathogenesis. Understanding the pathological, physiological and neuroprotective role of cyclooxygenase will contribute to the development of a therapy for the treatment or prevention of AD.
Keywords: alzheimers disease, cox, neuroinflammation, microglia, neuron, nsaids
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