Halliday et al1 recently reported that patients with Alzheimer disease (AD) with a history of exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) demonstrated enhanced cognitive function but did not show any reduction in pathological markers of disease in postmortem brain tissue. The lack of effect on senile plaque (SP) and neurofibrillary tangle formation is in agreement with findings we have published2 and is not unexpected since these processes likely take several decades to reach AD levels. However, their results contrast sharply with those of several other in vivo and in vitro studies, in which NSAIDs have been shown to reduce microglial activation associated with SP or exogenous Aβ protein.2-4 Since an effect of anti-inflammatory drugs on microglial cell activity is central to the inflammatory hypothesis of AD, we feel that critical evaluation of the negative result found by Halliday et al is warranted and offer the following possible explanations:
Mackenzie IRA, Munoz DG. Effect of Anti-inflammatory Medications on Neuropathological Findings in Alzheimer Disease. Arch Neurol. 2001;58(3):517–518. doi:
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