Evidence map›Paper›PMID 29993324›Full record

ArticleJournal of neurotrauma2019

Chronic White Matter Degeneration, but No Tau Pathology at One-Year Post-Repetitive Mild Traumatic Brain Injury in a Tau Transgenic Model.

Benoit Mouzon, Corbin Bachmeier, Joseph Ojo, Christopher Acker, Scott Ferguson, Gogce Crynen, Peter Davies, Michael Mullan, William Stewart, Fiona Crawford

Open access · greenAbstract read
In one paragraph

Article in Journal of neurotrauma, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

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  14. Repetitive Mild Closed Head Injury in Adolescent Mice Is Associated with Impaired Proteostasis, Neuroinflammation, and Tauopathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
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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

10 authors at 2 institutions in 1 country.

Benoit Mouzon1 Roskamp Institute , Sarasota, Florida.
Corbin Bachmeier1 Roskamp Institute , Sarasota, Florida.
Joseph Ojo1 Roskamp Institute , Sarasota, Florida.
Christopher Acker2 Feinstein Institute for Medical Research , Manhasset, New York.
Scott Ferguson1 Roskamp Institute , Sarasota, Florida.
Gogce Crynen1 Roskamp Institute , Sarasota, Florida.
Peter Davies2 Feinstein Institute for Medical Research , Manhasset, New York.
Michael Mullan1 Roskamp Institute , Sarasota, Florida.
William Stewart3 Department of Neuropathology, Laboratory Medicine Building, Queen Elizabeth University Hospital , Glasgow, Scotland.
Fiona Crawford1 Roskamp Institute , Sarasota, Florida.
Roskamp Institute · USFeinstein Institute for Medical Research · US

Funding

TBI: Uncovering Mechanisms of AD-like pathologyR01NS038104 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI SMITH, DOUGLAS HAMILTON · 1999 to 2020
$7.6M
Neuropathological Characterization of 'CTE'R01NS094003 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI Douglas Hamilton Smith, William Stewart · 2016 to 2026
$5.1M
NINDS NIH HHS R01 NS038104NINDS NIH HHS R01 NS094003
6 · The paper itself

Abstract

Tau pathology associated with chronic traumatic encephalopathy has been documented in the brains of individuals with a history of repetitive mild traumatic brain injury (r-mTBI). At this stage, the pathobiological role of tau in r-mTBI has not been extensively explored in appropriate pre-clinical models. Here, we describe the acute and chronic behavioral and histopathological effects of single and repetitive mild TBI (five injuries given at 48 h intervals) in young adult (3 months old) hTau mice that express all six isoforms of hTau on a null murine tau background. Animals exposed to r-mTBI showed impaired visuospatial learning in the Barnes maze test that progressively worsened from two weeks to 12 months post-injury, which was also accompanied by significant deficits in visuospatial memory consolidation at 12 months post-injury. In contrast, only marginal changes were observed in visuospatial learning at six and 12 months after single mTBI. Histopathological analyses revealed that hTau mice developed axonal injury, thinning of the corpus callosum, microgliosis and astrogliosis in the white matter at acute and chronic time points after injury. Tau immunohistochemistry and enzyme-linked immunosorbent assay data suggest, however, only transient, injury-dependent increases in phosphorylated tau in the cerebral cortex beneath the impact site and in the CA1/CA3 subregion of the hippocampus after single or r-mTBI. This study implicates white matter degeneration as a prominent feature of survival from mTBI, while the role of tau pathology in the neuropathological sequelae of TBI remains elusive.

Indexed as

AnimalsChronic Traumatic EncephalopathyDisease Models, AnimalHumansMaleMaze LearningMiceMice, TransgenicNerve Degenerationtau ProteinsWhite MatterMAPT protein, humantau Proteinsadult head injuryageanimal studiesaxonal injurybehavior

Identifiers

PMID29993324
PMCPMC6354615
OpenAlexW2866827747

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.