ArticleFrontiers in cellular neuroscience2022
Mild Traumatic Brain Injury-Induced Disruption of the Blood-Brain Barrier Triggers an Atypical Neuronal Response.
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 18 citations in OpenAlex.
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Transglutaminase 2 Deletion Enhances Astrocyte-to-Neuron Metabolic Support and Attenuates Subacute Pathology Following Repetitive Mild Traumatic Brain Injury.bioRxiv : the preprint server for biology · 2026Article
- Mild Traumatic Brain Injury as a Heterogeneous Neurological Disorder: Definition, Epidemiology, Neurobiology, and Clinical Course.Korean journal of neurotrauma · 2026Review
- Temporal and Spatial Patterns of Glial Activation After Unilateral Cortical Injury in Rats.Life (Basel, Switzerland) · 2026Article
- Shared neuropathological features of mild traumatic brain injury and anesthesia.Frontiers in neurology · 2026Review
- Cerebrospinal fluid mechanics across CNS barriers: from production, circulation, and clearance to mechanomedicine.Frontiers in neuroscience · 2026Review
- Modulating Cerebrospinal Fluid Composition in Neurodegenerative Processes: Modern Drug Delivery and Clearance Strategies.International journal of molecular sciences · 2025Review
- Diffuse traumatic brain injury induced stimulator of interferons (STING) signaling in microglia drives cortical neuroinflammation, neuronal dysfunction, and impaired cognition.Journal of neuroinflammation · 2025Article
- Diffuse Traumatic Brain Injury Induced Stimulator of Interferons (STING) Signaling in Microglia Drives Cortical Neuroinflammation, Neuronal Dysfunction, and Impaired Cognition.Research square · 2025Article
- "Proteinjury": a universal pathological mechanism mediated by cerebrospinal fluid in neurodegeneration and trauma.Frontiers in cell and developmental biology · 2025Review
- Shared inflammatory glial cell signature after stab wound injury, revealed by spatial, temporal, and cell-type-specific profiling of the murine cerebral cortex.Nature communications · 2024Article
- Repetitive head trauma and apoE4 induce chronic cerebrovascular alterations that impair tau elimination from the brain.Experimental neurology · 2024Article
- Trigeminal Sensitization in a Closed Head Model for Mild Traumatic Brain Injury.Journal of neurotrauma · 2024Article
- The missing hallmark of health: psychosocial adaptation.Cell stress · 2024Article
- Catalpol promotes hippocampal neurogenesis and synaptogenesis in rats after multiple cerebral infarctions by mitochondrial regulation: involvement of the Shh signaling pathway.Frontiers in pharmacology · 2024Article
- Sleep-associated insulin resistance promotes neurodegeneration.Molecular biology reports · 2023Review
- Aberrant accumulation of age- and disease-associated factors following neural probe implantation in a mouse model of Alzheimer's disease.Journal of neural engineering · 2023Article
- Commonly Overlooked Factors in Biocompatibility Studies of Neural Implants.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- The pathological potential of ependymal cells in mild traumatic brain injury.Frontiers in cellular neuroscience · 2023Review
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Mild TBI (mTBI), which affects 75% of TBI survivors or more than 50 million people worldwide each year, can lead to consequences including sleep disturbances, cognitive impairment, mood swings, and post-traumatic epilepsy in a subset of patients. To interrupt the progression of these comorbidities, identifying early pathological events is key. Recent studies have shown that microbleeds, caused by mechanical impact, persist for months after mTBI and are correlated to worse mTBI outcomes. However, the impact of mTBI-induced blood-brain barrier damage on neurons is yet to be revealed. We used a well-characterized mouse model of mTBI that presents with frequent and widespread but size-restricted damage to the blood-brain barrier to assess how neurons respond to exposure of blood-borne factors in this pathological context. We used immunohistochemistry and histology to assess the expression of neuronal proteins in excitatory and inhibitory neurons after mTBI. We observed that the expression of NeuN, Parvalbumin, and CamKII was lost within minutes in areas with blood-brain barrier disruption. Yet, the neurons remained alive and could be detected using a fluorescent Nissl staining even 6 months later. A similar phenotype was observed after exposure of neurons to blood-borne factors due to endothelial cell ablation in the absence of a mechanical impact, suggesting that entrance of blood-borne factors into the brain is sufficient to induce the neuronal atypical response. Changes in postsynaptic spines were observed indicative of functional changes. Thus, this study demonstrates That exposure of neurons to blood-borne factors causes a rapid and sustained loss of neuronal proteins and changes in spine morphology in the absence of neurodegeneration, a finding that is likely relevant to many neuropathologies.
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