ArticleJournal of neurotrauma2010
Genetic deletion and pharmacological inhibition of Nogo-66 receptor impairs cognitive outcome after traumatic brain injury in mice.
Article in Journal of neurotrauma, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Persistent increase of Nogo-A-positive cells and dynamic reduction in oligodendroglia lineage cells in white matter regions following experimental and clinical traumatic brain injury.Journal of neuropathology and experimental neurology · 2025Article
- NgR1 binding to reovirus reveals an unusual bivalent interaction and a new viral attachment protein.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- miR-182-5p Regulates Nogo-A Expression and Promotes Neurite Outgrowth of Hippocampal Neurons In Vitro.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Post-Traumatic Epilepsy and Comorbidities: Advanced Models, Molecular Mechanisms, Biomarkers, and Novel Therapeutic Interventions.Pharmacological reviews · 2022Review
- Peptide Pharmacological Approaches to Treating Traumatic Brain Injury: a Case for Arginine-Rich Peptides.Molecular neurobiology · 2017Review
- Nogo presence is inversely associated with shifts in cortical microglial morphology following experimental diffuse brain injury.Neuroscience · 2017Article
- The Controlled Cortical Impact Model: Applications, Considerations for Researchers, and Future Directions.Frontiers in neurology · 2016Review
- Chronic Histopathological and Behavioral Outcomes of Experimental Traumatic Brain Injury in Adult Male Animals.Journal of neurotrauma · 2015Review
- Nogo-A expression dynamically varies after spinal cord injury.Neural regeneration research · 2015Article
- Traumatic brain injury using mouse models.Translational stroke research · 2014Review
- Escalated handling of young C57BL/6 mice results in altered Morris water maze performance.Upsala journal of medical sciences · 2014Article
- Lacosamide improves outcome in a murine model of traumatic brain injury.Neurocritical care · 2013Article
- Inhibition of Nogo-66 receptor 1 enhances recovery of cognitive function after traumatic brain injury in mice.Journal of neurotrauma · 2013Article
- Lateralized response of dynorphin a peptide levels after traumatic brain injury.Journal of neurotrauma · 2012Article
- Indomethacin protects rats from neuronal damage induced by traumatic brain injury and suppresses hippocampal IL-1β release through the inhibition of Nogo-A expression.Journal of neuroinflammation · 2012Article
- Aging, synaptic dysfunction, and insulin-like growth factor (IGF)-1.The journals of gerontology. Series A, Biological sciences and medical sciences · 2012Review
- Genetic manipulation of cell death and neuroplasticity pathways in traumatic brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2012Review
- Hippocampal expression of myelin-associated inhibitors is induced with age-related cognitive decline and correlates with deficits of spatial learning and memory.Journal of neurochemistry · 2012Article
- Posttraumatic mossy fiber sprouting is related to the degree of cortical damage in three mouse strains.Epilepsy research · 2012Article
- Chinese Medicine's Intervention Effect on Nogo-A/NgR.Evidence-based complementary and alternative medicine : eCAM · 2012Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Functional recovery is markedly restricted following traumatic brain injury (TBI), partly due to myelin-associated inhibitors including Nogo-A, myelin-associated glycoprotein (MAG) and oligodendrocyte myelin glycoprotein (OMgp), that all bind to the Nogo-66 receptor-1 (NgR1). In previous studies, pharmacological neutralization of both Nogo-A and MAG improved outcome following TBI in the rat, and neutralization of NgR1 improved outcome following spinal cord injury and stroke in rodent models. However, the behavioral and histological effects of NgR1 inhibition have not previously been evaluated in TBI. We hypothesized that NgR1 negatively influences behavioral recovery following TBI, and evaluated NgR1(-/-) mice (NgR1(-/-) study) and, in a separate study, soluble NgR1 infused intracerebroventricularly immediately post-injury to neutralize NgR1 (sNgR1 study) following TBI in mice using a controlled cortical impact (CCI) injury model. In both studies, motor function, TBI-induced loss of tissue, and hippocampal beta-amyloid immunohistochemistry were not altered up to 5 weeks post-injury. Surprisingly, cognitive function (as evaluated with the Morris water maze at 4 weeks post-injury) was significantly impaired both in NgR1(-/-) mice and in mice treated with soluble NgR1. In the sNgR1 study, we evaluated hippocampal mossy fiber sprouting using the Timm stain and found it to be increased at 5 weeks following TBI. Neutralization of NgR1 significantly increased mossy fiber sprouting in sham-injured animals, but not in brain-injured animals. Our data suggest a complex role for myelin-associated inhibitors in the behavioral recovery process following TBI, and urge caution when inhibiting NgR1 in the early post-injury period.
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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.