ReviewJournal of neurology2004
The neuroprotective role of inflammation in nervous system injuries.
Review in Journal of neurology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
55 citing papers in PubMed, 146 citations in OpenAlex.
- The effects of Taurine supplementation on inflammatory markers and clinical outcomes in patients with traumatic brain injury: a double-blind randomized controlled trial.Nutrition journal · 2021Trial
- A model of new-onset refractory status epilepticus (NORSE) using intrahippocampal kainic acid in adolescent mice.Epilepsy research · 2026Article
- Cerebral and Peripheral Immune Cell Changes following Rodent Juvenile Traumatic Brain Injury.Brain sciences · 2024Article
- The inflammatory response to birth requires MyD88 and is driven by both mother and offspring.Brain, behavior, and immunity · 2024Article
- Cellular and Molecular Mechanisms and Innovative Neurostimulation Treatments in the Management of Traumatic Brain Injury.Journal of biotechnology and biomedicine · 2024Article
- Beyond an inflammatory mediator: Interleukin-1 in neurophysiology.Experimental physiology · 2023Review
- Extreme prematurity: Risk and resiliency.Current problems in pediatric and adolescent health care · 2022Review
- Urinary metabolomic signatures as indicators of injury severity following traumatic brain injury: A pilot study.IBRO neuroscience reports · 2021Article
- Treelet transform analysis to identify clusters of systemic inflammatory variance in a population with moderate-to-severe traumatic brain injury.Brain, behavior, and immunity · 2021Article
- Transplantation of R-GSIK scaffold with mesenchymal stem cells improves neuroinflammation in a traumatic brain injury model.Cell and tissue research · 2020Article
- Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions.Biomedicines · 2020Review
- Calpain inhibitor MDL28170 improves the transplantation-mediated therapeutic effect of bone marrow-derived mesenchymal stem cells following traumatic brain injury.Stem cell research & therapy · 2019Article
- The Potassium SK Channel Activator NS309 Protects Against Experimental Traumatic Brain Injury Through Anti-Inflammatory and Immunomodulatory Mechanisms.Frontiers in pharmacology · 2019Article
- STING-mediated type-I interferons contribute to the neuroinflammatory process and detrimental effects following traumatic brain injury.Journal of neuroinflammation · 2018Article
- Birth delivery mode alters perinatal cell death in the mouse brain.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- The microbiota influences cell death and microglial colonization in the perinatal mouse brain.Brain, behavior, and immunity · 2018Article
- Microglia and CNS Interleukin-1: Beyond Immunological Concepts.Frontiers in neurology · 2018Review
- Relationship Between Obesity, Alzheimer's Disease, and Parkinson's Disease: an Astrocentric View.Molecular neurobiology · 2017Review
- Optical coherence tomography and T cell gene expression analysis in patients with benign multiple sclerosis.Neural regeneration research · 2017Article
- In immune defense: redefining the role of the immune system in chronic disease.Dialogues in clinical neuroscience · 2017Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The contribution of inflammation to the pathogenesis of several nervous system disorders has long been established. Other observations, however, indicate that both inflammatory cells and mediators may also have beneficial functions, assisting in repair and recovery processes. There is compelling evidence to indicate that in the injured nervous system, as in other tissues, macrophages are needed at an early stage after injury in order for healing to take place. Likewise, activated T cells of a particular specificity can reduce the spread of damage. This neuroprotective effect of T cells may be caused, at least in part, by the production of neurotrophic factors such as neurotrophin-3 or brain-derived neurotrophic factor. Interestingly, recent findings indicate that immune cells are able to produce a variety of neurotrophic factors which promote neuronal survival and may also mediate anti-inflammatory effects. Numerous cytokines are induced after nervous system injuries. Some cytokines, such as TNF-alpha, IL-1 and IFN-gamma, are well known for their promotion of inflammatory responses. However, these cytokines also have immunosuppressive functions and their subsequent expression also assists in repair or recovery processes, suggesting a dual role for some pro-inflammatory cytokines. This should be clarified, as it may be crucial in the design of therapeutic strategies to target specific cytokine(s). Finally, there is a growing body of evidence to show that autoreactive IgM antibodies may constitute an endogenous system of tissue repair, and therefore prove of value as a therapeutic strategy. Available evidence would appear to indicate that the inflammatory response observed in several neurological conditions is more complex than previously thought. Therefore, the design of more effective therapies depends on a clear delineation of the beneficial and detrimental effects of inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.