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Anti‐inflammatory agents as a therapeutic approach to Alzheimer's disease
Abstract
Postmortem analyses of Alzheimer's disease (AD) brain tissue reveal reactive microglia expressing high levels of major histocompatibility complex (MHC) glycoproteins, immunoglobulin receptors, and complement receptors; small but significant numbers of T-lymphocytes infiltrating tissue; enhanced cytokine and cytokine receptor expression; and profuse immunoreactivity for complement proteins of the classic pathway colocalized with senile plaques, dystrophic neurites, and some neurofibrillary tangles. Protectin, clusterin, and vitronectin, three proteins designed to defend host cells against "bystander lysis" caused by the membrane attack complex of complement, are all expressed at high levels in AD tissue but not in normal tissue. Taken together, these findings indicate that immune-mediated autodestructive processes may occur in AD. In view of the urgency to find treatments for AD and disappointing results with the many classes of pharmacologic agents that have so far been given clinical trials, exploration of the effectiveness of anti-inflammatory agents may now be warranted.
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Cited by
Inflammation as a central mechanism in Alzheimer's disease
Kinney, J. W., Bemiller, S. M., Murtishaw, A. S., Leisgang, A. M., Salazar, A. M., & Lamb, B. T. (2018) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1016/j.trci.2018.06.014 · Cited by 2,253
“Unlike other risk factors and genetic causes of AD, neuroinflammation is not typically thought to be causal on its own but rather a result of one or more of the other AD pathologies or risk factors associated with AD and serves to increase the severity of the disease by exacerbating b-amyloid and tau pathologies [90,9…”
BackgroundMCGEER, P., & MCGEER, E. (1995) · Brain Research Reviews · doi:10.1016/0165-0173(95)00011-9 · Cited by 1,287
Self-citationThe amyloid hypothesis for Alzheimer’s disease: A critical reappraisal
Hardy, J. (2009) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2009.06181.x · Cited by 814
Lee, J. W., Lee, Y. K., Yuk, D. Y., Choi, D. Y., Ban, S. B., Oh, K. W., & Hong, J. T. (2008) · Journal of Neuroinflammation · doi:10.1186/1742-2094-5-37 · Cited by 772
History and progress of hypotheses and clinical trials for Alzheimer’s disease
Liu, P.-P., Xie, Y., Meng, X.-Y., & Kang, J.-S. (2019) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-019-0063-8 · Cited by 723
Metadata
- Authors
- McGeer, P. L., & Rogers, J.
- Venue
- Neurology
- Published
- 1992-02
- Volume
- 42
- Issue
- 2
- Pages
- 447-447
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2004053486
- Cited by
- 406
- References
- 0
- FWCI
- 15.84
- Type
- journal article
- Language
- en
- Open access
- closed
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- McGeer, P. L., & Rogers, J. (1992). Anti‐inflammatory agents as a therapeutic approach to Alzheimer's disease. Neurology. https://doi.org/10.1212/wnl.42.2.447
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.
