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Cited by 139Neuroinflammation and Neurodegeneration MechanismsTryptophan and brain disordersTraumatic Brain Injury and Neurovascular Disturbances

The DOI matches its Crossref record, with a small difference in title or year; 33 of the 34 references it cites were found in a registry or an index.

Interleukin‐1 in the Brain: Mechanisms of Action in Acute Neurodegeneration

PATEL, H. C., BOUTIN, H., ALLAN, S. M.·2003·Annals of the New York Academy of Sciences
DOI 10.1111/j.1749-6632.2003.tb03136.x
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Abstract

A bstract: Interleukin‐1 (IL‐1) exerts a number of diverse actions in the brain, and it is currently well accepted that it contributes to experimentally induced neurodegeneration. Much of this is based on studies using the IL‐1 receptor antagonist, which inhibits cell death caused by ischemia, brain injury, or excitotoxins. Our aim is to determine how and where in the brain IL‐1 acts to produce these effects. Most of the neurodegenerative effects of IL‐1 are thought to be through IL‐1β. However, we have data implicating IL‐1α in excitotoxic cell death. Furthermore mice lacking both IL‐1α and IL‐1β show dramatically reduced ischemic cell death, whereas deletion of IL‐1α or IL‐1β alone fails to modify damage. It has also been demonstrated that IL‐1 exacerbates ischemic injury in mice in the absence of the type I IL‐1 receptor, suggesting the existence of novel IL‐1 receptors in the brain. IL‐1 also dramatically exacerbates neuronal loss in response to intrastriatal administration of the excitotoxin AMPA in the rat brain, an effect accompanied by marked increases in cytokine expression in the frontoparietal cortex, which precedes subsequent cell death in this region. Intrastriatal AMPA also results in limbic seizures that are exacerbated by IL‐1, and we hypothesize, therefore, that IL‐1 exacerbates cell death through increased seizure activity. Therefore, IL‐1 appears to induce acute neurodegeneration through a number of mechanisms.

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Crossref · 10.1111/j.1749-6632.2003.tb03136.x

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Research works printed but not linked: 1

  1. Iannotti F., 1993, Interleukin 1b in focal cerebral ischaemia in rats, J. Cereb. Blood Flow Metab., 13, S125

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Metadata

Authors
PATEL, H. C., BOUTIN, H., & ALLAN, S. M.
Affiliations
University of Manchester (GB)
Corresponding author
ALLAN, S. M.
ORCID
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2003-05
Volume
992
Issue
1
Pages
39-47
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
DOI
10.1111/j.1749-6632.2003.tb03136.x
OpenAlex
W2021461507
Cited by
139
References
34
Citations by year
2026: 1 · 2025: 4 · 2024: 1 · 2023: 2 · 2022: 3 · 2021: 4 · 2020: 4 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 5 · 2015: 2 · 2014: 4 · 2013: 7 · 2012: 11
FWCI
1.73
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 999 d)
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
  • Research Explorer (The University of Manchester) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords
interleukin-1, interleukin-1 alpha, IL-1β, neurodegeneration, excitotoxic cell death, ischemic cell death, interleukin-1 receptor antagonist, IL-1 receptor type I, limbic seizures, cytokine expression, brain injury
MeSH terms
Acute Disease, Animals, Brain, Brain Injuries, Brain Ischemia, Disease Models, Animal, Humans, Interleukin-1, Nerve Degeneration, Recombinant Proteins, Seizures, Mice

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