ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2023
Tackling Neuroinflammation After Traumatic Brain Injury: Complement Inhibition as a Therapy for Secondary Injury.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 3 of them syntheses that pooled it.
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Who cites it
37 citing papers in PubMed, 3 syntheses or guidelines pooled it, 54 citations in OpenAlex.
- The Role of Neuroinflammation in Shaping Neuroplasticity and Recovery Outcomes Following Traumatic Brain Injury: A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Pooled it
- Comparison of Antioxidant Capacity and Network Pharmacology of Phloretin and Phlorizin against Neuroinflammation in Traumatic Brain Injury.Molecules (Basel, Switzerland) · 2023Pooled it
- Nanozyme-based therapeutic strategies for traumatic brain injury.International journal of pharmaceutics: X · 2026Review
- Semaglutide exerts neuroprotective effects by blocking the interleukin-17/NOD-like receptor family pyrin domain containing 3-mediated neuroinflammation pathway after traumatic brain injury.Neural regeneration research · 2026Article
- Complement in Traumatic Brain Injury: Linking Acute Injury to Chronic Neurodegeneration.European journal of immunology · 2026Review
- Inflammatory blood-based biomarkers to aid in the assessment and prognostication of traumatic brain injury: a TRACK-TBI study.Journal of neuroinflammation · 2026Article
- The Potential and Prospects of Hydrogel Applications in Traumatic Brain Injury Treatment.Current issues in molecular biology · 2026Review
- Topiramate protects against neuroinflammation in response to traumatic brain injury via activating Sirt1 signaling.Scientific reports · 2026Article
- Anti-inflammatory Effects of Synaptamide in the Peripheral Immune System in a Murine Model of Traumatic Brain Injury.Cell biochemistry and biophysics · 2026Article
- Coaxial nanofiber design for traumatic brain injury: a review and framework for phase-responsive therapeutics.Discover nano · 2026Review
- Molecular characterization ofOpen veterinary journal · 2026Article
- Th17 cells and IL-17A in traumatic brain injury: mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Risk of brain tumors following traumatic brain injury: A retrospective cohort study.Neurosurgical review · 2025Article
- Previous exposure to traumatic brain injury alters acute stress responses in mice.Scientific reports · 2025Article
- Recent advances in theranostic nanomaterials for overcoming traumatic brain injury.Journal of nanobiotechnology · 2025Review
- Elastin-like polypeptide delivery of an NF-kB inhibitor for treatment of juvenile mild TBI complicated by high-fat diet consumption.Experimental neurology · 2025Article
- The long-term influences of age at injury on neuroinflammation and neuronal apoptosis following traumatic brain injury in pediatric and adult mice.Clinical and experimental emergency medicine · 2025Article
- Complement Inhibition in Chronic Subdural Hematoma Fluid.Inflammation · 2025Article
- Traumatic Brian Injury (TBI) unraveled: molecular disruptions and therapeutic avenues.Inflammopharmacology · 2025Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a leading cause of mortality, sensorimotor morbidity, and neurocognitive disability. Neuroinflammation is one of the key drivers causing secondary brain injury after TBI. Therefore, attenuation of the inflammatory response is a potential therapeutic goal. This review summarizes the most important neuroinflammatory pathophysiology resulting from TBI and the clinical trials performed to attenuate neuroinflammation. Studies show that non-selective attenuation of the inflammatory response, in the early phase after TBI, might be detrimental and that there is a gap in the literature regarding pharmacological trials targeting specific pathways. The complement system and its crosstalk with the coagulation system play an important role in the pathophysiology of secondary brain injury after TBI. Therefore, regaining control over the complement cascades by inhibiting overshooting activation might constitute useful therapy. Activation of the complement cascade is an early component of neuroinflammation, making it a potential target to mitigate neuroinflammation in TBI. Therefore, we have described pathophysiological aspects of complement inhibition and summarized animal studies targeting the complement system in TBI. We also present the first clinical trial aimed at inhibition of complement activation in the early days after brain injury to reduce the risk of morbidity and mortality following severe TBI.
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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.