ArticleBrain : a journal of neurology2016
Attenuated traumatic axonal injury and improved functional outcome after traumatic brain injury in mice lacking Sarm1.
Article in Brain : a journal of neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 2 of them syntheses that pooled it.
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Who cites it
133 citing papers in PubMed, 2 syntheses or guidelines pooled it, 209 citations in OpenAlex.
- Mouse closed head traumatic brain injury replicates the histological tau pathology pattern of human disease: characterization of a novel model and systematic review of the literature.Acta neuropathologica communications · 2021Pooled it
- A Systematic Review of Closed Head Injury Models of Mild Traumatic Brain Injury in Mice and Rats.Journal of neurotrauma · 2019Pooled it
- Trial of Sodium Phenylbutyrate-Taurursodiol for Amyotrophic Lateral Sclerosis.The New England journal of medicine · 2020Trial
- Direct activation of SARM1 by dsDNA is not supported by biochemical and cellular evidence.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Nicotinamide Mononucleotide Adenylyltransferase 1 and NADMetabolites · 2026Review
- Boldine inhibits SARM1 NADase Activity and Preserves Axonal Integrity After Nerve Injury.bioRxiv : the preprint server for biology · 2026Article
- SARM1 activation promotes axonal degeneration via a two-step phase transition.Nature chemical biology · 2026Article
- Ferroptosis-Mediated Hippocampal Neuronal Loss Post-mTBI: Chromatin Accessibility Profiling and Single-Nucleus Transcriptomics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Hyperglycemia promotes SIRT3-mediated deacetylation of SARM1 to exacerbate diabetic peripheral neuropathy in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Mapping the secondary response to traumatic brain injury using spatial transcriptomics shows acute 4-aminopyridine treatment mitigates axonal and molecular pathology.Acta neuropathologica communications · 2026Article
- New mechanistic insight into SARM1 activation: TRIM32-mediated ubiquitination is a key lever that actuates SARM1's catalytic action, leading to axon degeneration and cell death.Frontiers in neural circuits · 2026Article
- Increased synaptic turnover in injured cortical axons: exploring the role of SARM1 ablation.Frontiers in synaptic neuroscience · 2026Article
- Astrocytic SIRT1 ameliorates cognitive deficits after traumatic brain injury via autophagy-mediated MEGF10 phagocytosis.Journal of neuroinflammation · 2025Article
- Deficiency of SARM1 attenuates neuronal injury and improves neurological performance in a photothrombotic stroke model.Molecular brain · 2025Article
- Article
- Review
- SARM1: The Checkpoint of Axonal Degeneration in the Nervous System Disorders.Molecular neurobiology · 2025Review
- Carnosol, a Rosemary Ingredient Discovered in a Screen for Inhibitors of SARM1-NADAntioxidants (Basel, Switzerland) · 2025Article
- Genetic Ablation of Sarm1 Mitigates Disease Acceleration after Traumatic Brain Injury in the SOD1Annals of neurology · 2025Article
- Transcranial Magnetic Stimulation Alleviates Spatial Learning and Memory Impairment by Inhibiting the Expression of SARM1 in Rats with Cerebral Ischemia-Reperfusion Injury.Neuromolecular medicine · 2025Article
73 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Axonal degeneration is a critical, early event in many acute and chronic neurological disorders. It has been consistently observed after traumatic brain injury, but whether axon degeneration is a driver of traumatic brain injury remains unclear. Molecular pathways underlying the pathology of traumatic brain injury have not been defined, and there is no efficacious treatment for traumatic brain injury. Here we show that mice lacking the mouse Toll receptor adaptor Sarm1 (sterile α/Armadillo/Toll-Interleukin receptor homology domain protein) gene, a key mediator of Wallerian degeneration, demonstrate multiple improved traumatic brain injury-associated phenotypes after injury in a closed-head mild traumatic brain injury model. Sarm1(-/-) mice developed fewer β-amyloid precursor protein aggregates in axons of the corpus callosum after traumatic brain injury as compared to Sarm1(+/+) mice. Furthermore, mice lacking Sarm1 had reduced plasma concentrations of the phophorylated axonal neurofilament subunit H, indicating that axonal integrity is maintained after traumatic brain injury. Strikingly, whereas wild-type mice exibited a number of behavioural deficits after traumatic brain injury, we observed a strong, early preservation of neurological function in Sarm1(-/-) animals. Finally, using in vivo proton magnetic resonance spectroscopy we found tissue signatures consistent with substantially preserved neuronal energy metabolism in Sarm1(-/-) mice compared to controls immediately following traumatic brain injury. Our results indicate that the SARM1-mediated prodegenerative pathway promotes pathogenesis in traumatic brain injury and suggest that anti-SARM1 therapeutics are a viable approach for preserving neurological function after traumatic brain injury.
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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.