ReviewNeurotoxicity research2003
Neuropathological and biochemical features of traumatic injury in the developing brain.
Review in Neurotoxicity research, 2003. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Pediatric Traumatic Brain Injury: Models, Therapeutics, and Outcomes.Advances in neurobiology · 2024Review
- Pre-clinical models in pediatric traumatic brain injury-challenges and lessons learned.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2017Review
- Detrimental or beneficial: the role of TRPM2 in ischemia/reperfusion injury.Acta pharmacologica Sinica · 2016Review
- Alpha II Spectrin breakdown products in immature Sprague Dawley rat hippocampus and cortex after traumatic brain injury.Brain research · 2014Article
- Contrasting neuropathology and functional recovery after spinal cord injury in developing and adult rats.Neuroscience bulletin · 2013Article
- Animal models of intellectual disability: towards a translational approach.Clinics (Sao Paulo, Brazil) · 2011Review
- Is age-dependent, ketamine-induced apoptosis in the rat somatosensory cortex influenced by temperature?Neuroscience · 2010Article
- Calpain 1 and Calpastatin expression is developmentally regulated in rat brain.Experimental neurology · 2009Article
- Role of animal studies in the design of clinical trials.Frontiers of neurology and neuroscience · 2009Review
- Mild traumatic brain injury to the infant mouse causes robust white matter axonal degeneration which precedes apoptotic death of cortical and thalamic neurons.Experimental neurology · 2008Article
- Brain development in rodents and humans: Identifying benchmarks of maturation and vulnerability to injury across species.Progress in neurobiologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trauma to the developing brain constitutes a poorly explored field. Some recent studies attempting to model and study pediatric head trauma, the leading cause of death and disability in the pediatric population, revealed interesting aspects and potential targets for future research. Trauma triggers both excitotoxic and apoptotic neurodegeneration in the developing rat brain. Excitotoxic neurodegeneration develops and subsides rapidly (within hours) whereas apoptotic cell death occurs in a delayed fashion over several days following the initial traumatic insult. Apoptotic neurodegeneration contributes in an age-dependent fashion to neuronal injury following head trauma, with the immature brain being exceedingly sensitive. In the most vulnerable ages the apoptosis contribution to the extent of traumatic brain damage far outweighs that of the excitotoxic component. Molecular and biochemical studies indicate that both extrinsic and intrinsic mechanisms are involved in pathogenesis of apoptotic cell death following trauma. Interestingly, in infant rats a pan-caspase inhibitor ameliorated apoptotic neurodegeneration with a therapeutic time window of up to 8 h after trauma. These results help explain unfavorable outcomes of very young pediatric head trauma patients and imply that regimens which target slow active forms of cell death may comprise a successful neuroprotective approach.
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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.