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Brain Inflammation in Alzheimer Disease and the Therapeutic Implications

McGeer, Edith G., McGeer, Patrick L.·1999·Current Pharmaceutical Design

Abstract

Immunohistochemical studies suggested the existence of a chronic inflammatory condition in affected regions of the brain in Alzheimer disease (AD). Since inflammation can be damaging to host tissue, it was hypothesized that antiinflammatory drugs might inhibit both the onset and the progression of AD. This hypothesis is supported by a number of epidemiological studies suggesting that the prevalence of AD in persons is reduced by 40 - 50% in persons using antiinflammatory drugs. In one small pilot trial in early AD, the nonsteroidal antiinflammatory drug indomethacin appeared to halt the progressive memory loss. Immunohistochemical and molecular biological studies on immune system components in AD brain are revealing the complexities of the innate immune reaction. This very complexity may offer points of therapeutic intervention for new types of antiinflammatory agents. The complement system, microglia and cytokines are key components. This review summarizes the present state of knowledge on the immune system elements found in AD brain.

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Metadata

Authors
McGeer, E. G., & McGeer, P. L.
Venue
Current Pharmaceutical Design
Published
1999-10
Volume
5
Issue
10
Pages
821-836
ISSN
1381-6128 (ISSN-L)
OpenAlex
W4316093067
Cited by
198
References
0
FWCI
9.69
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Brain Inflammation in Alzheimer Disease and the Therapeutic Implications. https://app.cochat.ai/papers/10.2174/1381612805666230111212056
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McGeer, E. G., & McGeer, P. L. (1999). Brain Inflammation in Alzheimer Disease and the Therapeutic Implications. Current Pharmaceutical Design. https://doi.org/10.2174/1381612805666230111212056

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.