ArticleJournal of neuropathology and experimental neurology2013
Diffuse traumatic axonal injury in the optic nerve does not elicit retinal ganglion cell loss.
Article in Journal of neuropathology and experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Eyes Are the Windows to the Soul: Reviewing the Possible Use of the Retina to Indicate Traumatic Brain Injury.International journal of molecular sciences · 2025Review
- Cortical Morphometric Similarity Remodeling in Traumatic Brain Injury Links Cognitive Impairments with Transcriptional Changes and Type-Specific Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Visual Impairment in Pre-Clinical Models of Mild Traumatic Brain Injury.Journal of neurotrauma · 2024Review
- Model matters: Differential outcomes in traumatic optic neuropathy pathophysiology between blunt and blast-wave mediated head injuries.Experimental neurology · 2024Article
- Traumatic Brain Injury Induces Microglial and Caspase3 Activation in the Retina.International journal of molecular sciences · 2023Article
- Review: Emerging Eye-Based Diagnostic Technologies for Traumatic Brain Injury.IEEE reviews in biomedical engineering · 2023Review
- Traumatic axonal injury: neuropathological features, postmortem diagnostic methods, and strategies.Forensic science, medicine, and pathology · 2022Review
- Article
- Visual Dysfunction after Repetitive Mild Traumatic Brain Injury in a Mouse Model and Ramifications on Behavioral Metrics.Journal of neurotrauma · 2021Article
- Article
- From biomechanics to pathology: predicting axonal injury from patterns of strain after traumatic brain injury.Brain : a journal of neurology · 2021Article
- A Novel NAD Signaling Mechanism in Axon Degeneration and its Relationship to Innate Immunity.Frontiers in molecular biosciences · 2021Review
- Visual Outcomes in Experimental Rodent Models of Blast-Mediated Traumatic Brain Injury.Frontiers in molecular neuroscience · 2021Review
- Assessment of necroptosis in the retina in a repeated primary ocular blast injury mouse model.Experimental eye research · 2020Article
- Emergence of SARM1 as a Potential Therapeutic Target for Wallerian-type Diseases.Cell chemical biology · 2020Review
- Microglial process convergence on axonal segments in health and disease.Neuroimmunology and neuroinflammation · 2020Article
- Expression of transcription factors divides retinal ganglion cells into distinct classes.The Journal of comparative neurology · 2019Article
- Intensity Specific Repetitive Mild Traumatic Brain Injury Evokes an Exacerbated Burden of Neocortical Axonal Injury.Journal of neuropathology and experimental neurology · 2018Article
- Mild Traumatic Brain Injury Induces Structural and Functional Disconnection of Local Neocortical Inhibitory Networks via Parvalbumin Interneuron Diffuse Axonal Injury.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Acute vitreoretinal trauma and inflammation after traumatic brain injury in mice.Annals of clinical and translational neurology · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Much of the morbidity after traumatic brain injury (TBI) is associated with traumatic axonal injury (TAI). Although most TAI studies focus on corpus callosum white matter, the visual system has received increased interest. To assess visual system TAI, we developed a mouse model of optic nerve TAI. It is unknown, however, whether this TAI causes retinal ganglion cell (RGC) death. To address this issue, YFP (yellow fluorescent protein)-16 transgenic mice were subjected to mild TBI and followed from 2 to 28 days. Neither TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling)-positive or cleaved caspase-3-immunoreactive RGCs were observed from 2 to 28 days after TBI. Quantification of immunoreactivity of Brn3a, an RGC marker, demonstrated no RGC loss; parallel electron microscopic analysis confirmed RGC viability. Persistent RGC survival was also consistent with the finding of reorganization in the proximal axonal segments after TAI, wherein microglia/macrophages remained inactive. In contrast, activated microglia/macrophages closely enveloped the distal disconnected, degenerating axonal segments at 7 to 28 days after injury, thereby confirming that this model consistently evoked TAI followed by disconnection. Collectively, these data provide novel insight into the evolving pathobiology associated with TAI that will form a foundation for future studies exploring TAI therapy and its downstream 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.