The treatment of Alzheimers disease is undoubtedly one of the greatest challenges of modern medicine and pharmacology. Affecting millions of people, Alzheimers disease has become a major social problem. Several theories have been proposed to account for its pathogenesis. Possibly, the “amyloid cascade hypothesis” is the dominant one. However, the “inflammation hypothesis” also contributes to the pathogenesis of the disease. Thus, this study intends to describe the role of neuroinflammation in Alzheimers disease, regarding its cellular and molecular components, and to examine if the use of non-steroidal anti-inflammatory drugs could be an effective “weapon” in the battle against it.
Keywords: Alzheimer's disease, inflammation, pharmacology, non-steroidal anti-inflammatory drugs, NSAIDs, APP, presenilin-1, presenilin-2, apolipoprotein E, APOE, Pen2, ubiquitin-proteasome pathway, clearance, Neuroinflammation, CD36, TLR4, synaptic plasticity, cyclooxygenase, COX, EP1-4, chlamydophila, helicobacter pylori, borrelia burgdorferi, Tg2576, R-flurbiprofen, ibuprofen, indomethacin, naproxen, flurbiprofen, CHF5022, CHF5074, ADAPT, MCI
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