Activation of microglia surrounding amyloid plaques in AD brains could be a double-edged sword. On one hand, activated microglia can release harmful inflammatory substances. On the other hand, activated microglia can scavenge toxic Aft. Microglial activation can be inhibited by non-steroidal anti-inflammatory drugs (NSAIDs). Epidemiological studies show that NSAID usage is associated with a lower risk of AD . However, clinical trials of NSAIDs in AD patients have been largely disappointing . The lack of efficacy of NSAIDs can be ascribed to its potential use only for prevention but not treatment, the inappropriate doses or drugs chosen in the trials or a faulty hypothesis. In contrast to NSAIDs, Aft immunotherapy may depend at least in part on the activation of microglia . Aft immunotherapy is currently being investigated in clinical trials (Tables 1 and 2). It has been proposed that there maybe multiple activation states of microglia: some could be associated with release of toxic inflammatory substances while others with the beneficial removal of Aft (Morgan 2006). A more precise characterization of these different states of activation may lead to more precise and efficacious treatments targeting microglial activation.
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