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

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
Open this paper in CoChat — free account

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.

Integrity signals

Registry

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

Cites

33 of 33 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Inflammatory cytokines influence neuronal development and apoptosis, and both stress and inflammatory cytokine activity may adversely influence neurogenesis and neuroplasticity.

    “Inflammatory cytokines have repeatedly been observed to influence both neuronal development and apoptosis (Chawla-Sarkar et al., 2003, Hayley et al., 2005) (Mehler and Kessler, 1997, Zhao and Schwartz, 1998), (Peng et al., 2008, Anisman, 2009, Koo et al., 2010b). In fact, both stress and subsequent inflammatory cytokine activity may adversely influence neurogenesis and neuroplasticity (Patel et al”

    From Inflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications (2013) · cites this paper as Patel et al., 2003

Cites

Flagged first, then by citations

1 of the 34 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Related

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 › 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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review