Evidence map›Paper›PMID 27274873›Full record

ArticleNeural plasticity2016

Astrocyte Hypertrophy Contributes to Aberrant Neurogenesis after Traumatic Brain Injury.

Clark Robinson, Christopher Apgar, Lee A Shapiro

Open access · goldAbstract read
In one paragraph

Article in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 68 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Clark RobinsonDepartment of Surgery, Texas A&M University Health Science Center, College of Medicine, Temple, TX 76504, USA; Central Texas Veterans Health Care System, Temple, TX 76504, USA.
Christopher ApgarDepartment of Surgery, Texas A&M University Health Science Center, College of Medicine, Temple, TX 76504, USA; Central Texas Veterans Health Care System, Temple, TX 76504, USA.
Lee A ShapiroDepartment of Surgery, Texas A&M University Health Science Center, College of Medicine, Temple, TX 76504, USA; Central Texas Veterans Health Care System, Temple, TX 76504, USA; Department of Neurosurgery, Neuroscience Research Institute, Scott & White Hospital, Temple, TX 76508, USA.
Texas A&M University · USScott & White Memorial Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a widespread epidemic with severe cognitive, affective, and behavioral consequences. TBIs typically result in a relatively rapid inflammatory and neuroinflammatory response. A major component of the neuroinflammatory response is astrocytes, a type of glial cell in the brain. Astrocytes are important in maintaining the integrity of neuronal functioning, and it is possible that astrocyte hypertrophy after TBIs might contribute to pathogenesis. The hippocampus is a unique brain region, because neurogenesis persists in adults. Accumulating evidence supports the functional importance of these newborn neurons and their associated astrocytes. Alterations to either of these cell types can influence neuronal functioning. To determine if hypertrophied astrocytes might negatively influence immature neurons in the dentate gyrus, astrocyte and newborn neurons were analyzed at 30 days following a TBI in mice. The results demonstrate a loss of radial glial-like processes extending through the granule cell layer after TBI, as well as ectopic growth and migration of immature dentate neurons. The results further show newborn neurons in close association with hypertrophied astrocytes, suggesting a role for the astrocytes in aberrant neurogenesis. Future studies are needed to determine the functional significance of these alterations to the astrocyte/immature neurons after TBI.

Indexed as

AnimalsAstrocytesBrain Injuries, TraumaticCell ProliferationDentate GyrusDisease Models, AnimalMiceNeurogenesisNeurons

Identifiers

PMID27274873
PMCPMC4870378
OpenAlexW2345554436

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.