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
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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“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
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Metadata
- Authors
- PATEL, H. C., BOUTIN, H., & ALLAN, S. M.
- Affiliations
- University of Manchester (GB)
- Corresponding author
- ALLAN, S. M.
- 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
- 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
- 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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