ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2021
Traumatic Brain Injury Causes Chronic Cortical Inflammation and Neuronal Dysfunction Mediated by Microglia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 245 papers, 4 of them syntheses that pooled it.
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Who cites it
245 citing papers in PubMed, 4 syntheses or guidelines pooled it, 379 citations in OpenAlex.
- Microglia in Post-Traumatic Brain Injury (TBI) Cognitive Impairment: From Pathological Changes to Therapeutic Approaches.CNS neuroscience & therapeutics · 2025Pooled it
- The Role of Neuroinflammation in Shaping Neuroplasticity and Recovery Outcomes Following Traumatic Brain Injury: A Systematic Review.International journal of molecular sciences · 2024Pooled it
- A Meta-analysis of Predicting Disorders of Consciousness After Traumatic Brain Injury by Machine Learning Models.Alpha psychiatry · 2024Pooled it
- Exploring the biological basis of acupuncture treatment for traumatic brain injury: a review of evidence from animal models.Frontiers in cellular neuroscience · 2024Pooled it
- P2X7 receptor-mediated IL-1β release by human brain tissue: the impact of CNS-penetrant potential therapeutics.Brain : a journal of neurology · 2026Article
- Curcumin relieves gas explosion-induced brain injury via TLR4-mediated M2 polarization of microglia.Brain, behavior, & immunity - health · 2026Article
- Pediatric Mild Traumatic Brain Injury and Concussion: Modern Pathophysiological Insights, Diagnostic Advances, and Active Management Protocols.Brain sciences · 2026Review
- Temporal transcriptomic remodeling after controlled cortical impact reveals delayed AQP4/SNTA1 expression imbalance associated with ion-homeostatic remodeling.bioRxiv : the preprint server for biology · 2026Article
- Therapeutic Potential of Allicin in Multi-System Inflammatory Diseases.Current issues in molecular biology · 2026Review
- Traumatic Brain Injury and the Road to Alzheimer's Disease.Biomedicines · 2026Review
- Psilocybin restores behavior and 5-HTCell reports. Medicine · 2026Article
- Pediatric traumatic brain injury elicits acute neuroinflammation and long-term changes in social, cognitive, and decision-making behaviors in male and female rats.bioRxiv : the preprint server for biology · 2026Article
- Repeated mild spinal cord contusions exacerbate tauopathy development in PS19 mice.Acta neuropathologica communications · 2026Article
- FcγR- and CD9-dependent synapse-engulfing microglia in the thalamus drive cognitive impairment following cortical brain damage in mice.Nature communications · 2026Article
- Microglia-specific NLRP3 inhibition mitigates hippocampal neuroinflammation and cognitive deficits after hemorrhagic shock with resuscitation.Behavioral and brain functions : BBF · 2026Article
- Type I interferon signaling in microglia drives synaptic engulfment and neuronal loss following traumatic brain injury.Research square · 2026Article
- Brain-engrafted monocyte-derived macrophages from blood and skull-bone marrow exhibit distinct properties.Neuron · 2026Article
- Inflammatory blood-based biomarkers to aid in the assessment and prognostication of traumatic brain injury: a TRACK-TBI study.Journal of neuroinflammation · 2026Article
- The effects of physical exercise on inflammation-induced maladaptive neuroplasticity in post-traumatic headache.Neuroscience · 2026Review
- IL-3 Modulates Microglia Polarization and Attenuates Neuroinflammation in Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
185 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Traumatic brain injury (TBI) can lead to significant neuropsychiatric problems and neurodegenerative pathologies, which develop and persist years after injury. Neuroinflammatory processes evolve over this same period. Therefore, we aimed to determine the contribution of microglia to neuropathology at acute [1 d postinjury (dpi)], subacute (7 dpi), and chronic (30 dpi) time points. Microglia were depleted with PLX5622, a CSF1R antagonist, before midline fluid percussion injury (FPI) in male mice and cortical neuropathology/inflammation was assessed using a neuropathology mRNA panel. Gene expression associated with inflammation and neuropathology were robustly increased acutely after injury (1 dpi) and the majority of this expression was microglia independent. At 7 and 30 dpi, however, microglial depletion reversed TBI-related expression of genes associated with inflammation, interferon signaling, and neuropathology. Myriad suppressed genes at subacute and chronic endpoints were attributed to neurons. To understand the relationship between microglia, neurons, and other glia, single-cell RNA sequencing was completed 7 dpi, a critical time point in the evolution from acute to chronic pathogenesis. Cortical microglia exhibited distinct TBI-associated clustering with increased type-1 interferon and neurodegenerative/damage-related genes. In cortical neurons, genes associated with dopamine signaling, long-term potentiation, calcium signaling, and synaptogenesis were suppressed. Microglial depletion reversed the majority of these neuronal alterations. Furthermore, there was reduced cortical dendritic complexity 7 dpi, reduced neuronal connectively 30 dpi, and cognitive impairment 30 dpi. All of these TBI-associated functional and behavioral impairments were prevented by microglial depletion. Collectively, these studies indicate that microglia promote persistent neuropathology and long-term functional impairments in neuronal homeostasis after 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.