ArticleNature communications2025
The transcriptional response of cortical neurons to concussion reveals divergent fates after injury.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Activating Transcription Factor 3 in Pain: A Molecular Regulator and Emerging Biomarker.Genes · 2026Review
- Single-Cell Profiling Reveals a Protective WNT5A-ATF3-FOSB Signaling Axis in Hair Follicle Stem Cells During Androgenetic Alopecia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Impact-acceleration head injury results in optic neuropathy in the thirteen-lined ground squirrel.Communications biology · 2026Article
- Inflammasome adaptor ASC promotes sustained neuroinflammation and mild cognitive impairment in a closed-head injury model.The Journal of clinical investigation · 2026Article
- From Traumatic Brain Injury to Alzheimer's Disease: Multilevel Biomechanical, Neurovascular, and Molecular Mechanisms with Emerging Therapeutic Directions.International journal of molecular sciences · 2026Review
- The Role of MRI in Debunking the Fallacy of "Mild" Traumatic Brain Injury.Journal of magnetic resonance imaging : JMRI · 2026Review
- Synaptic control of retinal ganglion cell survival and axon regeneration.Molecular neurodegeneration · 2026Review
- Maladaptive immunity to the microbiota promotes neuronal hyperinnervation and itch via IL-17A.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Nanocatalytic Neuroprotection and Neurological Recovery Post-Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A Bioinformatic Study of Genetics Involved in Determining Mild Traumatic Brain Injury Severity and Recovery.Biomedicines · 2025Article
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10 authors.
Funding
Abstract
Traumatic brain injury (TBI) is a risk factor for neurodegeneration, however little is known about how this kind of injury alters neuron subtypes. In this study, we follow neuronal populations over time after a single mild TBI (mTBI) to assess long ranging consequences of injury at the level of single, transcriptionally defined neuronal classes. We find that the stress-responsive Activating Transcription Factor 3 (ATF3) defines a population of cortical neurons after mTBI. Using an inducible reporter linked to ATF3, we genetically mark these damaged cells to track them over time. We find that a population in layer V undergoes cell death acutely after injury, while another in layer II/III survives long term and remains electrically active. To investigate the mechanism controlling layer V neuron death, we genetically silenced candidate stress response pathways. We found that the axon injury responsive dual leucine zipper kinase (DLK) is required for the layer V neuron death. This work provides a rationale for targeting the DLK signaling pathway as a therapeutic intervention for traumatic brain injury. Beyond this, our approach to track neurons after a mild, subclinical injury can inform our understanding of neuronal susceptibility to repeated impacts.
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