ArticleJournal of neurotrauma2023
Traumatic Axonal Injury in the Optic Nerve: The Selective Role of SARM1 in the Evolution of Distal Axonopathy.
Article in Journal of neurotrauma, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Metabolic Symbiosis and Vulnerability in the CNS Axon-Myelin Unit.Cellular and molecular neurobiology · 2026Review
- Recovery of Retinal Terminal Fields after Traumatic Brain Injury: Evidence of Collateral Sprouting and Sexual Dimorphism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Alterations of Bioactive Lipid Profiles in the Retina Following Traumatic Optic Neuropathy in Mice.Biomolecules · 2025Article
- Recovery of retinal terminal fields after traumatic brain injury: evidence of collateral sprouting and sexual dimorphism.bioRxiv : the preprint server for biology · 2025Article
- SARM1: The Checkpoint of Axonal Degeneration in the Nervous System Disorders.Molecular neurobiology · 2025Review
- 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
- Downregulation of SARM1 Protects Retinal Ganglion Cell Axonal and Somal Degeneration Via JNK Activation in a Glaucomatous Model of Ocular Hypertension.Investigative ophthalmology & visual science · 2024Article
- Visual Impairment in Pre-Clinical Models of Mild Traumatic Brain Injury.Journal of neurotrauma · 2024Review
- Programmed axon death: a promising target for treating retinal and optic nerve disorders.Eye (London, England) · 2024Review
- Loss of Sarm1 reduces retinal ganglion cell loss in chronic glaucoma.Acta neuropathologica communications · 2024Article
- NADAntioxidants & redox signaling · 2023Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic axonal injury (TAI), thought to be caused by rotational acceleration of the head, is a prevalent neuropathology in traumatic brain injury (TBI). TAI in the optic nerve is a common finding in multiple blunt-force TBI models and hence a great model to study mechanisms and treatments for TAI, especially in view of the compartmentalized anatomy of the visual system. We have previously shown that the somata and the proximal, but not distal, axons of retinal ganglion cells (RGC) respond to DLK/LZK blockade after impact acceleration of the head (IA-TBI). Here, we explored the role of the sterile alpha and TIR-motif containing 1 (SARM1), the key driver of Wallerian degeneration (WD), in the progressive breakdown of distal and proximal segments of the optic nerve following IA-TBI with high-resolution morphological and classical neuropathological approaches. Wild type and
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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.