ArticleMolecular medicine (Cambridge, Mass.)2015
CD40-CD40 Ligand Pathway is a Major Component of Acute Neuroinflammation and Contributes to Long-term Cognitive Dysfunction after Sepsis.
Article in Molecular medicine (Cambridge, Mass.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- Long-Term Cognitive Outcomes After Sepsis: a Translational Systematic Review.Molecular neurobiology · 2019Pooled it
- TheBioMed research international · 2018Trial
- Hippocampal cytopathology orchestrates post-septic cognitive dysfunction.Metabolic brain disease · 2026Review
- The Role of Dopamine Signaling and Neuroinflammation in Age-Related Cognitive Dysfunction.Brain and behavior · 2026Article
- The crosstalk between blood-brain barrier and neural cells: bidirectional regulation of brain function and pathology.Biochemistry and biophysics reports · 2026Review
- Biomarkers of sepsis associated encephalopathy: a bibliometric and visualized analysis.Frontiers in neurology · 2025Article
- Amelioration of Neurochemical Alteration and Memory and Depressive Behavior in Sepsis by Allopurinol, a Tryptophan 2,3-Dioxygenase Inhibitor.CNS & neurological disorders drug targets · 2024Article
- Effect of Systemic Inflammation in the CNS: A Silent History of Neuronal Damage.International journal of molecular sciences · 2023Review
- Inhibition of platelet activation suppresses reactive enteric glia and mitigates intestinal barrier dysfunction during sepsis.Molecular medicine (Cambridge, Mass.) · 2022Article
- Mitochondrial protective effects caused by the administration of mefenamic acid in sepsis.Journal of neuroinflammation · 2022Article
- Inhibition of platelet activation suppresses reactive enteric glia and mitigates intestinal barrier dysfunction during sepsis.Molecular medicine (Cambridge, Mass.) · 2022Article
- Pathogenesis of sepsis-associated encephalopathy: more than blood-brain barrier dysfunction.Molecular biology reports · 2022Review
- Sepsis modulates cortical excitability and alters the local and systemic hemodynamic response to seizures.Scientific reports · 2022Article
- Differential Gene Sets Profiling in Gram-Negative and Gram-Positive Sepsis.Frontiers in cellular and infection microbiology · 2022Article
- Current Understanding of Long-Term Cognitive Impairment After Sepsis.Frontiers in immunology · 2022Review
- Sepsis-Associated Encephalopathy and Blood-Brain Barrier Dysfunction.Inflammation · 2021Review
- Downregulation of CD40L-CD40 attenuates seizure susceptibility and severity of seizures.Scientific reports · 2021Article
- Generation of mitochondrial reactive oxygen species is controlled by ATPase inhibitory factor 1 and regulates cognition.PLoS biology · 2021Article
- Stanniocalcin 1 Inhibits the Inflammatory Response in Microglia and Protects Against Sepsis-Associated Encephalopathy.Neurotoxicity research · 2021Article
- Sepsis and Cerebral Dysfunction: BBB Damage, Neuroinflammation, Oxidative Stress, Apoptosis and Autophagy as Key Mediators and the Potential Therapeutic Approaches.Neurotoxicity research · 2021Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-associated encephalopathy (SAE) is associated with an increased rate of morbidity and mortality. It is not understood what the exact mechanism is for the brain dysfunction that occurs in septic patients, but brain inflammation and oxidative stress are a possible theory. Such events can occur through the alteration of molecules that perpetuate the inflammatory response. Thus, it is possible to postulate that CD40 may be involved in this process. The aim of this work is to evaluate the role of CD40-CD40L pathway activation in brain dysfunction associated with sepsis in an animal model. Microglia activation induces the upregulation of CD40-CD40L, both in vitro and in vivo. The inhibition of microglia activation decreases levels of CD40-CD40L in the brain and decreases brain inflammation, oxidative damage and blood brain barrier dysfunction. Despite this, anti-CD40 treatment does not improve mortality in this model. However, it is able to improve long-term cognitive impairment in sepsis survivors. In conclusion, there is a major involvement of the CD40-CD40L signaling pathway in long-term brain dysfunction in an animal model of sepsis.
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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.