Evidence map›Paper›PMID 18440507›Full record

ArticleExperimental neurology2008

Mild traumatic brain injury to the infant mouse causes robust white matter axonal degeneration which precedes apoptotic death of cortical and thalamic neurons.

K Dikranian, R Cohen, C Mac Donald, Y Pan, D Brakefield, P Bayly, A Parsadanian

Open access · greenAbstract readComparative Study
In one paragraph

Article in Experimental neurology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. A multi-staged neuropeptide response to traumatic brain injury.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Cell Death and Recovery in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020
    Review
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

K DikranianDepartment of Anatomy and Neurobiology, Washington University, St. Louis, 660 S. Euclid Avenue, St. Louis, MO 63110, USA.
R Cohen
C Mac Donald
Y Pan
D Brakefield
P Bayly
A Parsadanian
Hope Center for Neurological Disorders · USWashington University in St. Louis · US

Funding

GDNF: EFFECTS ON NORMAL AND DEGENERATING MOTOR NEURONSR01NS042794 · NINDS · WASHINGTON UNIVERSITY · PI PARSADANIAN, ALEXANDER S · 2002 to 2006
$1.5M
NINDS NIH HHS NS042794NINDS NIH HHS R01 NS042794
6 · The paper itself

Abstract

The immature brain in the first several years of childhood is very vulnerable to trauma. Traumatic brain injury (TBI) during this critical period often leads to neuropathological and cognitive impairment. Previous experimental studies in rodent models of infant TBI were mostly concentrated on neuronal degeneration, while axonal injury and its relationship to cell death have attracted much less attention. To address this, we developed a closed controlled head injury model in infant (P7) mice and characterized the temporospatial pattern of axonal degeneration and neuronal cell death in the brain following mild injury. Using amyloid precursor protein (APP) as marker of axonal injury we found that mild head trauma causes robust axonal degeneration in the cingulum/external capsule as early as 30 min post-impact. These levels of axonal injury persisted throughout a 24 h period, but significantly declined by 48 h. During the first 24 h injured axons underwent significant and rapid pathomorphological changes. Initial small axonal swellings evolved into larger spheroids and club-like swellings indicating the early disconnection of axons. Ultrastructural analysis revealed compaction of organelles, axolemmal and cytoskeletal defects. Axonal degeneration was followed by profound apoptotic cell death in the posterior cingulate and retrosplenial cortex and anterior thalamus which peaked between 16 and 24 h post-injury. At early stages post-injury no evidence of excitotoxic neuronal death at the impact site was found. At 48 h apoptotic cell death was reduced and paralleled with the reduction in the number of APP-labeled axonal profiles. Our data suggest that early degenerative response to injury in axons of the cingulum and external capsule may cause disconnection between cortical and thalamic neurons, and lead to their delayed apoptotic death.

Indexed as

Age FactorsAnimalsAnimals, NewbornApoptosisAxonsBrain InjuriesCell DeathCerebral CortexMiceMice, TransgenicNerve DegenerationNerve Fibers, MyelinatedNeuronsThalamus

Identifiers

PMID18440507
PMCPMC2486437
OpenAlexW1990339002

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.