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The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective
Open accessAbstract
Elevation of the proinflammatory cytokine Interleukin-1 (IL-1) is an integral part of the local tissue reaction to central nervous system (CNS) insult. The discovery of increased IL-1 levels in patients following acute injury and in chronic neurodegenerative disease laid the foundation for two decades of research that has provided important details regarding IL-1's biology and function in the CNS. IL-1 elevation is now recognized as a critical component of the brain's patterned response to insults, termed neuroinflammation, and of leukocyte recruitment to the CNS. These processes are believed to underlie IL-1's function in the setting of acute brain injury, where it has been ascribed potential roles in repair as well as in exacerbation of damage. Explorations of IL-1's role in chronic neurodegenerative disease have mainly focused on Alzheimer disease (AD), where indirect evidence has implicated it in disease pathogenesis. However, recent observations in animal models challenge earlier assumptions that IL-1 elevation and resulting neuroinflammatory processes play a purely detrimental role in AD, and prompt a need for new characterizations of IL-1 function. Potentially adaptive functions of IL-1 elevation in AD warrant further mechanistic studies, and provide evidence that enhancement of these effects may help to alleviate the pathologic burden of disease.
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“Elevated levels of IL-1β in the brain can itself induce neuroinflammation, neurotoxicity and learning and memory impairment [55, 74].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [74]
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Metadata
- Authors
- Shaftel, S. S., Griffin, W. S. T., & O'Banion, M. K.
- Affiliations
- University of Rochester Medicine (US)
- University of Arkansas for Medical Sciences (US)
- ORCID
- Griffin, W Sue T
- Venue
- Journal of Neuroinflammation
- Published
- 2008-02-26
- Volume
- 5
- Issue
- 1
- Pages
- 7-7
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC2335091
- OpenAlex
- W2015186493
- Cited by
- 565
- References
- 158
- Citations by year
- 2026: 22 · 2025: 49 · 2024: 47 · 2023: 55 · 2022: 36 · 2021: 43 · 2020: 42 · 2019: 34 · 2018: 23 · 2017: 28 · 2016: 21 · 2015: 30 · 2014: 27 · 2013: 32 · 2012: 25
- FWCI
- 1.46
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R21NS048522)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- interleukin-1, neuroinflammation, Alzheimer's disease, inflammatory cytokines, acute brain injury, neurodegenerative diseases, leukocyte recruitment
- MeSH terms
- Alzheimer Disease, Animals, Central Nervous System, Encephalitis, Humans, Interleukin-1, Leukocytes
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