ArticleJournal of neurotrauma2022
Mild Traumatic Brain Injury/Concussion Initiates an Atypical Astrocyte Response Caused by Blood-Brain Barrier Dysfunction.
Article in Journal of neurotrauma, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 48 citations in OpenAlex.
- Traumatic Brain Injury and the Road to Alzheimer's Disease.Biomedicines · 2026Review
- Cortical subpial aging-related tau astrogliopathy in older adult men who participated in youth amateur American-style football.Journal of neuropathology and experimental neurology · 2026Article
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- Fast ripple-delta coupling as an early biomarker for post-traumatic epileptogenesis in repetitive brain injury.Epilepsia open · 2026Article
- Pathological Roles of Astrocytes in Traumatic Brain Injury.CNS neuroscience & therapeutics · 2026Review
- The kynurenine pathway in pediatric "mild-to-moderate" traumatic brain injury: translational insights from a prospective human study and a large-animal model.Brain, behavior, and immunity · 2026Article
- Shared neuropathological features of mild traumatic brain injury and anesthesia.Frontiers in neurology · 2026Review
- Mild traumatic brain injury promotes chronic cerebrovascular inflammation and glymphatic suppression.Molecular neurodegeneration advances · 2026Article
- Fast Ripple-Delta Coupling as Early Biomarker for Post-Traumatic Epileptogenesis in Repetitive Brain Injury.bioRxiv : the preprint server for biology · 2025Article
- Concussion Disrupts Sleep in Adolescents: A Systematic Review and Meta-Analysis.Clocks & sleep · 2025Review
- Blood-brain barrier disruption: a pervasive driver and mechanistic link between traumatic brain injury and Alzheimer's disease.Translational neurodegeneration · 2025Review
- Extracellular cold-inducible RNA-binding protein in CNS injury: molecular insights and therapeutic approaches.Journal of neuroinflammation · 2025Review
- Article
- The NERD model: reflex circuit dysfunction as a systems-level driver of persistent post-concussion symptoms.Frontiers in systems neuroscience · 2025Article
- From Physiology to Pathology of Astrocytes: Highlighting Their Potential as Therapeutic Targets for CNS Injury.Neuroscience bulletin · 2025Review
- Assessment of Blood-Brain Barrier Integrity Using Dyes and Tracers.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Imaging Techniques for the Analysis of the Blood-Brain Barrier and Gliovascular Unit Dysfunction.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Neuroinflammatory Response in the Traumatic Brain Injury: An Update.Neurochemical research · 2024Review
- Organoids and chimeras: the hopeful fusion transforming traumatic brain injury research.Acta neuropathologica communications · 2024Review
- The potential of gene delivery for the treatment of traumatic brain injury.Journal of neuroinflammation · 2024Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Mild traumatic brain injury/concussion (mTBI) accounts for 70-90% of all reported TBI cases and causes long-lasting neurological consequences in 10-40% of patients. Recent clinical studies revealed increased blood-brain barrier (BBB) permeability in mTBI patients, which correlated with secondary damage after mTBI. However, the cascade of cellular events initiated by exposure to blood-borne factors resulting in sustained damage is not fully understood. We previously reported that astrocytes respond atypically to mTBI, rapidly losing many proteins essential to their homeostatic function, while classic scar formation does not occur. Here, we tested the hypothesis that mTBI-induced BBB damage causes atypical astrocytes through exposure to blood-borne factors. Using an mTBI mouse model, two-photon imaging, an endothelial cell-specific genetic ablation approach, and serum-free primary astrocyte cultures, we demonstrated that areas with atypical astrocytes coincide with BBB damage and that exposure of astrocytes to plasma proteins is sufficient to initiate loss of astrocyte homeostatic proteins. Although mTBI resulted in frequent impairment of both physical and metabolic BBB properties and leakage of small-sized blood-borne factors, deposition of the coagulation factor fibrinogen or vessel rupture were rare. Surprisingly, even months after mTBI, BBB repair did not occur in areas with atypical astrocytes. Together, these findings implicate that even relatively small BBB disturbances are sustained long term, and render nearby astrocytes dysfunctional, likely at the cost of neuronal health and function.
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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.