ArticleJournal of neurotrauma2013
Inhibition of Nogo-66 receptor 1 enhances recovery of cognitive function after traumatic brain injury in mice.
Article in Journal of neurotrauma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Article
- Active constituent of Polygala tenuifolia attenuates cognitive deficits by rescuing hippocampal neurogenesis in APP/PS1 transgenic mice.BMC complementary medicine and therapies · 2021Article
- Knockdown of Lingo-1 by short hairpin RNA promotes cognitive function recovery in a status convulsion model.3 Biotech · 2021Article
- NgR1 pathway expression in cerebral ischemic Sprague-Dawley rats with cognitive impairment.Iranian journal of basic medical sciences · 2021Article
- Acute effects of human protein S administration after traumatic brain injury in mice.Neural regeneration research · 2020Article
- Apolipoprotein E promotes white matter remodeling via the Dab1-dependent pathway after traumatic brain injury.CNS neuroscience & therapeutics · 2020Article
- The TRIM protein Mitsugumin 53 enhances survival and therapeutic efficacy of stem cells in murine traumatic brain injury.Stem cell research & therapy · 2019Article
- Use of Diffusional Kurtosis Imaging and Dynamic Contrast-Enhanced MR Imaging to Predict Posttraumatic Epilepsy in Rabbits.AJNR. American journal of neuroradiology · 2018Article
- 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
- A Shift from a Pivotal to Supporting Role for the Growth-Associated Protein (GAP-43) in the Coordination of Axonal Structural and Functional Plasticity.Frontiers in cellular neuroscience · 2017Review
- Severity-Dependent Long-Term Spatial Learning-Memory Impairment in a Mouse Model of Traumatic Brain Injury.Translational stroke research · 2016Article
- Anti-Nogo-A Immunotherapy Does Not Alter Hippocampal Neurogenesis after Stroke in Adult Rats.Frontiers in neuroscience · 2016Article
- Old dog, new tricks: the attentional set-shifting test as a novel cognitive behavioral task after controlled cortical impact injury.Journal of neurotrauma · 2014Article
- Traumatic Brain Injury pathophysiology and treatments: early, intermediate, and late phases post-injury.International journal of molecular sciences · 2013Review
- Resveratrol Alleviates Cognitive Impairment in Chronic Cerebral Hypoperfusion by Targeting Lingo-1, NgR1, p75, and RhoA/ROCK-2 Pathways.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Central nervous system (CNS) axons recover poorly following injury because of the expression of myelin-derived inhibitors of axonal outgrowth such as Nogo, myelin-associated glycoprotein (MAG), and oligodendrocyte-myelin glycoprotein (OMgp), all of which bind to the Nogo-66 receptor 1 (NgR1). Herein we examine the role of NgR1 in the recovery of motor and cognitive function after traumatic brain injury (TBI) using a controlled cortical impact (CCI) model in NgR1 knockout (KO) and wild-type (WT) mice. Four weeks post-injury, scores on the Novel Object Recognition test were significantly increased in NgR1 KO mice compared with WT mice (p<0.05), but motor behavior test scores did not differ significantly between the two groups. Nissl staining showed that NgR1 KO mice had less brain injury volume 2 weeks after CCI (p<0.05). Histological analysis revealed more doublecortin (DCX+) cells (p<0.01) and more Ki-67+ cells in the contralateral dentate gyrus (DG) (p<0.05) 2 weeks after CCI in NgR1 KO mice than in WT. Furthermore, DCX+ cells still retained their longer processes in KO mice (p<0.01) 4 weeks following trauma. The number of bromodeoxyuridine (BrdU)+ cells did not differ between the two groups at 4 weeks post-trauma, but KO mice had higher numbers of cells that co-stained with NeuN, a marker of mature neurons. Increased transcription of growth-associated protein (GAP)-43 in both the injured and contralateral sides of the hippocampus (both p<0.05) was detected in NgR1 KO mice relative to WT. These data suggest that NgR1 negatively influences plasticity and cognitive recovery after TBI.
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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.