The inflammatory hypothesis of Alzheimer's disease (AD) arose from a combination of
epidemiological and neurobiological evidence. The finding of an inverse association
between AD onset and prior use of anti-inflammatory drugs in co-twin control studies
suggested the possibility that exposure to these drugs might prevent or delay the
initial onset of AD symptoms (
1
). The discovery of a range of inflammatory processes in the AD brain—from activated
microglia to cytokines and the complement cascade—further supported the notion that
anti-inflammatory treatment might slow the progression of AD, even after onset (
2
,
3
). During the past 10 years this optimistic hypothesis has been sobered by a series
of negative randomized controlled trials of anti-inflammatory agents, including a
glucocorticoid therapy (
4
), nonsteroidal anti-inflammatory drugs (
5
,
6
,
7
,
8
), and hydroxychloroquine (
9
) for AD or the prodromal condition of mild cognitive impairment (MCI). Despite the
failure of these trials, interest in novel anti-inflammatory strategies for AD treatment
continues (
10
).To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
September 18,
2008
Received:
September 17,
2008
Identification
Copyright
© 2008 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
