ArticleJournal of neuroinflammation2014
Evaluating the levels of interleukin-1 family cytokines in sporadic amyotrophic lateral sclerosis.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02325375 (Inflammation in Amyotrophic Lateral Sclerosis - a Study of Soluble Cluster of Differentiation 163 in the Cerebrospinal Fluid), which is not on this map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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.
Inflammation in Amyotrophic Lateral Sclerosis - a Study of Soluble Cluster of Differentiation 163 in the Cerebrospinal Fluid
Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Immunobiological Properties and Clinical Applications of Interleukin-38 for Immune-Mediated Disorders: A Systematic Review Study.International journal of molecular sciences · 2021Pooled it
- Innate immune crosstalk in ALS/FTD pathogenesis.Cell insight · 2026Review
- Article
- Anti-Neuroinflammatory and Anti-Inflammatory Effects of the NLRP3 Inhibitor NT-0796 in Subjects with Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- The Emerging Role of the Brain-Gut Axis in Amyotrophic Lateral Sclerosis: Pathogenesis, Mechanisms, and Therapeutic Perspectives.International journal of molecular sciences · 2025Review
- Alzheimer's disease neuropathology and its estimation with fluid and imaging biomarkers.Molecular neurodegeneration · 2025Review
- Restoring Homeostasis: Treating Amyotrophic Lateral Sclerosis by Resolving Dynamic Regulatory Instability.International journal of molecular sciences · 2025Article
- Unveiling amyotrophic lateral sclerosis complexity: insights from proteomics, metabolomics and microbiomics.Brain communications · 2025Review
- Inflammasomes in neurodegenerative diseases.Translational neurodegeneration · 2024Review
- Decoding Neurodegeneration: A Review of Molecular Mechanisms and Therapeutic Advances in Alzheimer's, Parkinson's, and ALS.International journal of molecular sciences · 2024Review
- Cell-mediated cytotoxicity within CSF and brain parenchyma in spinal muscular atrophy unaltered by nusinersen treatment.Nature communications · 2024Article
- Article
- Eomesodermin expression in CD4CNS neuroscience & therapeutics · 2024Article
- A Potential Role of Interleukin-5 in the Pathogenesis and Progression of Amyotrophic Lateral Sclerosis: A New Molecular Perspective.International journal of molecular sciences · 2024Article
- The role of NLRP3 inflammasome in aging and age-related diseases.Immunity & ageing : I & A · 2024Review
- Inflammasomes in neurological disorders - mechanisms and therapeutic potential.Nature reviews. Neurology · 2024Review
- Brain-Gut-Microbiota Axis in Amyotrophic Lateral Sclerosis: A Historical Overview and Future Directions.Aging and disease · 2024Review
- Molecular Activation of NLRP3 Inflammasome by Particles and Crystals: A Continuing Challenge of Immunology and Toxicology.Annual review of pharmacology and toxicology · 2024Review
- Article
- Role of neuroinflammation in neurodegeneration development.Signal transduction and targeted therapy · 2023Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAmyotrophic lateral sclerosis (ALS) is a progressive motor neuron disease leading to the death of affected individuals within years. The involvement of inflammation in the pathogenesis of neurodegenerative diseases, including ALS, is increasingly recognized but still not well understood. The aim of this study is to evaluate the levels of inflammation-related IL-1 family cytokines (IL-1β, IL-18, IL-33, IL-37) and their endogenous inhibitors (IL-1Ra, sIL-1R2, IL-18BP, sIL-1R4) in patients with sporadic ALS (sALS),
methodsSera were collected from 144 patients (125 patients were characterized by disease form, duration, and disability, using the revised ALS functional rating scale (ALSFRS-R) and from 40 matched controls. Cerebrospinal fluid (CSF) was collected from 54 patients with sALS and 65 patients with other non-infectious non-oncogenic diseases as controls. Cytokines and inhibitors were measured by commercial ELISA.
resultsAmong the IL-1 family cytokines tested total IL-18, its endogenous inhibitor IL-18BP, and the active form of the cytokine (free IL-18) were significantly higher in the sALS sera than in controls. No correlation between these soluble mediators and different clinical forms of sALS or the clinical setting of the disease was found. IL-18BP was the only mediator detectable in the CSF of patients.
conclusionsAmong the IL-1 family cytokines, only IL-18 correlates with this disease and may therefore have a pathological role in sALS. The increase of total IL-18 suggests the activation of IL-18-cleaving inflammasome. Whether IL-18 upregulation in circulation of sALS patients is a consequence of inflammation or one of the causes of the pathology still needs to be addressed.
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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.