Cyclooxygenase and inflammation in Alzheimer's disease: experimental approaches and clinical interventions.
Many epidemiological studies suggest that use of non-steroidal anti-inflammatory drugs (NSAIDs) delay or slow the clinical expression of Alzheimer's disease (AD). While it has been demonstrated that neurodegeneration in AD is accompanied by specific inflammatory mechanisms, including activation of the complement cascade and the accumulation and activation of microglia, the mechanism by which NSAIDs might affect these or other pathophysiological processes relevant to AD has been unclear. New evidence that cyclooxygenase (COX) is involved in neurodegeneration along with the development of selective COX inhibitors has led to renewed interest in the therapeutic potential of NSAIDs in AD.
Department of Psychiatry, Brookdale Center for Molecular Biology and Fishberg Center for Neurobiology, The Mount Sinai School of Medicine, New York, NY, USA.
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Pasinetti
D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D001921:Brain / Q000378:metabolism / Q000473:pathology; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use*; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000473:pathology; D007527:Isoenzymes / Q000378:metabolism; D008565:Membrane Proteins; D018384:Oxidative Stress; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*
D000893:Anti-Inflammatory Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases