ArticleNeurotoxicity research2021
Acute Traumatic Brain Injury-Induced Neuroinflammatory Response and Neurovascular Disorders in the Brain.
Article in Neurotoxicity research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses 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
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Who cites it
27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.
- Pooled it
- New Insight of Circular RNAs' Roles in Central Nervous System Post-Traumatic Injury.Frontiers in neuroscience · 2021Pooled it
- Neurocardiac consequences of traumatic brain injury: integrating neuroimmune, autonomic, and cerebrovascular mechanisms.Frontiers in immunology · 2026Review
- The Relationship Between Inflammation and the Development of Cerebral Ischaemia and Hypoxia in Traumatic Brain Injury-A Narrative Review.International journal of molecular sciences · 2025Review
- Traumatic Brain Injury and Alzheimer's Disease: A Shared Neurovascular Hypothesis.Neuroscience insights · 2025Review
- Serum Zonulin, Claudin-5, junction Adhesion Molecule-A, Occludin and Tricellulin levels in children with autism spectrum disorder.International journal of developmental disabilities · 2025Article
- Neuroinflammatory Response in the Traumatic Brain Injury: An Update.Neurochemical research · 2024Review
- Nanoparticle targeting strategies for traumatic brain injury.Journal of neural engineering · 2024Review
- Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain.Experimental neurology · 2024Review
- Cerebral hypoperfusion exacerbates vascular dysfunction after traumatic brain injury.Experimental neurology · 2024Article
- Review
- Mild traumatic brain injury induces pericyte detachment independent of stroke vulnerability.Neuroscience letters · 2024Article
- Traumatic Brain Injury in the Long-COVID Era.Neurotrauma reports · 2024Review
- Sex-dependent temporal changes in astrocyte-vessel interactions following diffuse traumatic brain injury in rats.Frontiers in physiology · 2024Article
- Neurovascular unit, neuroinflammation and neurodegeneration markers in brain disorders.Frontiers in cellular neuroscience · 2024Review
- TIMP2 ameliorates blood-brain barrier disruption in traumatic brain injury by inhibiting Src-dependent VE-cadherin internalization.The Journal of clinical investigation · 2023Article
- Antidiabetic Drugs Can Reduce the Harmful Impact of Chronic Smoking on Post-Traumatic Brain Injuries.International journal of molecular sciences · 2023Article
- Altered endocannabinoid metabolism compromises the brain-CSF barrier and exacerbates chronic deficits after traumatic brain injury in mice.Experimental neurology · 2023Article
- Degranulation of Murine Resident Cochlear Mast Cells: A Possible Factor Contributing to Cisplatin-Induced Ototoxicity and Neurotoxicity.International journal of molecular sciences · 2023Article
- Role of hyperbaric oxygen therapy in PDGF-BB-mediated astrogliosis in traumatic brain injury rats associated with ERK1/2 signaling pathway inhibition.European journal of medical research · 2023Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Acute traumatic brain injury (TBI) leads to neuroinflammation, neurodegeneration, cognitive decline, psychological disorders, increased blood-brain barrier (BBB) permeability, and microvascular damage in the brain. Inflammatory mediators secreted from activated glial cells, neurons, and mast cells are implicated in the pathogenesis of TBI through secondary brain damage. Abnormalities or damage to the neurovascular unit is the indication of secondary injuries in the brain after TBI. However, the precise mechanisms of molecular and ultrastructural neurovascular alterations involved in the pathogenesis of acute TBI are not yet clearly understood. Moreover, currently, there are no precision-targeted effective treatment options to prevent the sequelae of TBI. In this study, mice were subjected to closed head weight-drop-induced acute TBI and evaluated neuroinflammatory and neurovascular alterations in the brain by immunofluorescence staining or quantitation by enzyme-linked immunosorbent assay (ELISA) procedure. Mast cell stabilizer drug cromolyn was administered to inhibit the neuroinflammatory response of TBI. Results indicate decreased level of pericyte marker platelet-derived growth factor receptor-beta (PDGFR-β) and BBB-associated tight junction proteins junctional adhesion molecule-A (JAM-A) and zonula occludens-1 (ZO-1) in the brains 7 days after weight-drop-induced acute TBI as compared with the brains from sham control mice indicating acute TBI-associated BBB/tight junction protein disruption. Further, the administration of cromolyn drug significantly inhibited acute TBI-associated decrease of PDGFR-β, JAM-A, and ZO-1 in the brain. These findings suggest that acute TBI causes BBB/tight junction damage and that cromolyn administration could protect this acute TBI-induced brain damage as well as its long-time consequences.
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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.