ArticleNeural plasticity2012
Mouse brain PSA-NCAM levels are altered by graded-controlled cortical impact injury.
Article in Neural plasticity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Immature Neurons in the Postnatal Brain: Markers, Modulation, and Involvement in Normal and Aberrant Plasticity.International journal of molecular sciences · 2026Review
- Single Nucleotide Polymorphism in Cell Adhesion Molecule L1 Affects Learning and Memory in a Mouse Model of Traumatic Brain Injury.International journal of molecular sciences · 2024Article
- Protective Effect of Lutein/Zeaxanthin Isomers in Traumatic Brain Injury in Mice.Neurotoxicity research · 2021Article
- Distinct and dementia-related synaptopathy in the hippocampus after military blast exposures.Brain pathology (Zurich, Switzerland) · 2021Article
- Accumulation of PSA-NCAM marks nascent neurodegeneration in the dorsal hippocampus after neonatal hypoxic-ischemic brain injury in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Exploratory, cognitive, and depressive-like behaviors in adult and pediatric mice exposed to controlled cortical impact.Clinical and experimental emergency medicine · 2019Article
- Development of a systems-based in situ multiplex biomarker screening approach for the assessment of immunopathology and neural tissue plasticity in male rats after traumatic brain injury.Journal of neuroscience research · 2018Article
- Preclinical Models of Traumatic Brain Injury: Emerging Role of Glutamate in the Pathophysiology of Depression.Frontiers in pharmacology · 2018Review
- Alterations in neurovascular coupling following acute traumatic brain injury.Neurophotonics · 2017Article
- Brain injury results in lower levels of melatonin receptors subtypes MT1 and MT2.Neuroscience letters · 2017Article
- Found in translation: Understanding the biology and behavior of experimental traumatic brain injury.Neuroscience and biobehavioral reviews · 2015Review
- A human anti-polysialic acid antibody as a potential treatment to improve function in multiple sclerosis patients.Journal of nature and science · 2015Article
- Endogenous neural stem/progenitor cells stabilize the cortical microenvironment after traumatic brain injury.Journal of neurotrauma · 2015Article
- Influence of the extracellular matrix on endogenous and transplanted stem cells after brain damage.Frontiers in cellular neuroscience · 2014Review
- Neuronal adhesion and synapse organization in recovery after brain injury.Future neurology · 2013Article
- Establishing a novel knock-in mouse line for studying neuronal cytoplasmic dynein under normal and pathologic conditions.Cytoskeleton (Hoboken, N.J.) · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a worldwide endemic that results in unacceptably high morbidity and mortality. Secondary injury processes following primary injury are composed of intricate interactions between assorted molecules that ultimately dictate the degree of longer-term neurological deficits. One comparatively unexplored molecule that may contribute to exacerbation of injury or enhancement of recovery is the posttranslationally modified polysialic acid form of neural cell adhesion molecule, PSA-NCAM. This molecule is a critical modulator of central nervous system plasticity and reorganization after injury. In this study, we used controlled cortical impact (CCI) to produce moderate or severe TBI in the mouse. Immunoblotting and immunohistochemical analysis were used to track the early (2, 24, and 48 hour) and late (1 and 3 week) time course and location of changes in the levels of PSA-NCAM after TBI. Variable and heterogeneous short- and long-term increases or decreases in expression were found. In general, alterations in PSA-NCAM levels were seen in the cerebral cortex immediately after injury, and these reductions persisted in brain regions distal to the primary injury site, especially after severe injury. This information provides a starting point to dissect the role of PSA-NCAM in TBI-related pathology and recovery.
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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.