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There is long-standing interest in the association between inflammation and Alzheimer disease (AD), driven by overwhelming evidence that brain inflammation (e.g., neuroinflammation) is a prominent feature of AD pathology, that nonsteroidal anti-inflammatory drugs may lower AD risk, and that some inflammatory gene loci are linked to AD.1 Yet the mechanisms by which inflammation contributes to disease pathogenesis are complex and how inflammation might be manipulated for therapeutic benefit remains elusive. One key is to recognize that inflammation may have different roles depending on whether it arises within the brain or from processes occurring in the periphery.
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Editorial, page 478
See page 486
- © 2014 American Academy of Neurology
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