Evidence map›Paper›PMID 30963638›Full record

ReviewJournal of internal medicine2019

Modelling human pathology of traumatic brain injury in animal models.

M Risling, D Smith, T D Stein, E P Thelin, E R Zanier, M Ankarcrona, P Nilsson

Abstract readReview
In one paragraph

Review in Journal of internal medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Article
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  12. Article
  13. Aβ1-6Molecular psychiatry · 2023
    Article
  14. Brain Trauma Imaging.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2023
    Article
  15. Review
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  18. Article
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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.

M RislingDepartment of Neuroscience, Karolinska Institutet, Solna, Sweden.
D SmithDepartment of Neurosurgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
T D SteinVA Boston Healthcare System, Boston, MA, USA.
E P ThelinDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-2338-4364
E R ZanierDepartment of Neuroscience, Mario Negri Institute, IRCCS Milano, Milano, Italy.
M AnkarcronaDivision of Neurogeriatrics, Department of Neurobiology, Care Science and Society, Center for Alzheimer Research, Karolinska Institutet, Solna, Sweden.
P NilssonDivision of Neurogeriatrics, Department of Neurobiology, Care Science and Society, Center for Alzheimer Research, Karolinska Institutet, Solna, Sweden.ORCID 0000-0001-6450-0870

Funding

Neuropathological Characterization of 'CTE'R01NS094003 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI Douglas Hamilton Smith, William Stewart · 2016 to 2026
$5.1M
Detection and Mechanisms of Mild Traumatic Brain InjuryR01NS092398 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI SMITH, DOUGLAS HAMILTON · 2015 to 2019
$1.9M
The neuropathology of mild traumatic brain injury in Alzheimer's diseaseI01CX001038 · VA · EDITH NOURSE ROGERS MEMORIAL VETERANS HOSPITAL · PI STEIN, THOR · 2015 to 2022
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CSRD VA I01 CX001038NINDS NIH HHS R01 NS092398NINDS NIH HHS R01 NS094003
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is caused by a head impact with a force exceeding regular exposure from normal body movement which the brain normally can accommodate. People affected include, but are not restricted to, sport athletes in American football, ice hockey, boxing as well as military personnel. Both single and repetitive exposures may affect the brain acutely and can lead to chronic neurodegenerative changes including chronic traumatic encephalopathy associated with the development of dementia. The changes in the brain following TBI include neuroinflammation, white matter lesions, and axonal damage as well as hyperphosphorylation and aggregation of tau protein. Even though the human brain gross anatomy is different from rodents implicating different energy transfer upon impact, especially rotational forces, animal models of TBI are important tools to investigate the changes that occur upon TBI at molecular and cellular levels. Importantly, such models may help to increase the knowledge of how the pathologies develop, including the spreading of tau pathologies, and how to diagnose the severity of the TBI in the clinic. In addition, animal models are helpful in the development of novel biomarkers and can also be used to test potential disease-modifying compounds in a preclinical setting.

Indexed as

Disease Models, AnimalAnimalsBrain Injuries, TraumaticHumansanimal modelsaxonal damagechronic traumatic encephalopathyneuroinflammationtautraumatic brain injury

Identifiers

PMID30963638
PMCPMC9351987

What OpenQuestion holds

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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.