The presence of even half the inflammatory mediators that have been demonstrated to be present and upregulated in the AD brain would signify to a peripheral inflammation biologist that a pathophysiologically relevant inflammatory attack was ongoing. The issue now is not whether or not inflammatory damage occurs in AD, but how it should be treated. As a secondary response to Aβ, neurofibrillary tangles and neurodegeneration, AD inflammation would obviously best be dealt with by removing the pathologies that stimulate it. However, we are still at some remove from being able to do this, whereas there are a number of conventional anti-inflammatory drugs that are widely available now. By understanding the basic science of AD neuroinflammation, particularly the inflammatory mediators that are present, we should be better able to make rational choices with regard to the most appropriate anti-inflammatory agents to test.
|Original language||English (US)|
|Number of pages||8|
|State||Published - 2000|