Evidence map›Paper›PMID 26857506›Full record

ArticleThe American journal of pathology2016

Dendritic Spine Loss and Chronic White Matter Inflammation in a Mouse Model of Highly Repetitive Head Trauma.

Charisse N Winston, Anastasia Noël, Aidan Neustadtl, Maia Parsadanian, David J Barton, Deepa Chellappa, Tiffany E Wilkins, Andrew D Alikhani, David N Zapple, Sonia Villapol and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 2 pooled it
9.2field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.

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  19. Aberrant cortical spine dynamics after concussive injury are reversed by integrated stress response inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 2 countries.

Charisse N WinstonLaboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia.
Anastasia NoëlDepartment of Psychiatry and Neurosciences, Université Laval, Quebec City, Quebec, Canada.
Aidan NeustadtlLaboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia.
Maia ParsadanianLaboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia.
David J BartonLaboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia.
Deepa ChellappaLaboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia.
Tiffany E WilkinsLaboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia.
Andrew D AlikhaniLaboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia.
David N ZappleLaboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia.
Sonia VillapolLaboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia.
Emmanuel PlanelDepartment of Psychiatry and Neurosciences, Université Laval, Quebec City, Quebec, Canada; Research Center of CHU of Québec, Neurosciences, Quebec, Canada. Electronic address: emmanuel@planel.org.
Mark P BurnsLaboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia. Electronic address: mpb37@georgetown.edu.
Georgetown University · USGeorgetown University Medical Center · USUniversité Laval · CA

Funding

Predoctoral Training in Intergrative NeuroscienceT32NS041231 · NINDS · GEORGETOWN UNIVERSITY · PI Ludise Malkova, Ashley S VanMeter · 2001 to 2026
$6.8M
Training in Neural Injury &PlasticityT32NS041218 · NINDS · GEORGETOWN UNIVERSITY · PI MARK P BURNS, Kathleen Anne Maguire-Zeiss · 2001 to 2026
$3.5M
The role of apoE and APOE genotype in amyloid-beta clearance after TBIR01NS081068 · NINDS · GEORGETOWN UNIVERSITY · PI BURNS, MARK P · 2013 to 2017
$1.8M
The role of Abeta in injury-induced cell deathR03NS067417 · NINDS · GEORGETOWN UNIVERSITY · PI BURNS, MARK P · 2010 to 2011
$152k
NINDS NIH HHS R01 NS081068NINDS NIH HHS R03 NS067417NINDS NIH HHS T32 NS041218NINDS NIH HHS T32NS041218NINDS NIH HHS T32 NS041231
6 · The paper itself

Abstract

Mild traumatic brain injury (mTBI) is an emerging risk for chronic behavioral, cognitive, and neurodegenerative conditions. Athletes absorb several hundred mTBIs each year; however, rodent models of repeat mTBI (rmTBI) are often limited to impacts in the single digits. Herein, we describe the effects of 30 rmTBIs, examining structural and pathological changes in mice up to 365 days after injury. We found that single mTBI causes a brief loss of consciousness and a transient reduction in dendritic spines, reflecting a loss of excitatory synapses. Single mTBI does not cause axonal injury, neuroinflammation, or cell death in the gray or white matter. Thirty rmTBIs with a 1-day interval between each mTBI do not cause dendritic spine loss; however, when the interinjury interval is increased to 7 days, dendritic spine loss is reinstated. Thirty rmTBIs cause white matter pathology characterized by positive silver and Fluoro-Jade B staining, and microglial proliferation and activation. This pathology continues to develop through 60 days, and is still apparent at 365 days, after injury. However, rmTBIs did not increase β-amyloid levels or tau phosphorylation in the 3xTg-AD mouse model of Alzheimer disease. Our data reveal that single mTBI causes a transient loss of synapses, but that rmTBIs habituate to repetitive injury within a short time period. rmTBI causes the development of progressive white matter pathology that continues for months after the final impact.

Indexed as

AmyloidAnimalsBehavior, AnimalBrain ConcussionBrain InjuriesCraniocerebral TraumaDendritic SpinesDisease Models, AnimalFluoresceinsGolgi ApparatusHumansInflammationMaleMaze LearningMiceMice, Inbred C57BLAmyloidFluoresceinsfluoro jadeMapt protein, mousetau Proteins

Identifiers

PMID26857506
PMCPMC4816714
OpenAlexW2256655086

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.