Evidence map›Paper›PMID 23826235›Full record

ArticlePloS one2013

Astrocyte-Specific Overexpression of Insulin-Like Growth Factor-1 Protects Hippocampal Neurons and Reduces Behavioral Deficits following Traumatic Brain Injury in Mice.

Sindhu K Madathil, Shaun W Carlson, Jennifer M Brelsfoard, Ping Ye, A Joseph D'Ercole, Kathryn E Saatman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.7field-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

61 citing papers in PubMed, 98 citations in OpenAlex.

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  19. Preclinical and clinical evidence of IGF-1 as a prognostic marker and acute intervention with ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  20. Review

1 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

6 authors at 2 institutions in 1 country.

Sindhu K MadathilSpinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky, United States of America.
Shaun W Carlson
Jennifer M Brelsfoard
Ping Ye
A Joseph D'Ercole
Kathryn E Saatman
University of Kentucky · USUniversity of North Carolina at Chapel Hill · US

Funding

UK Spinal Cord &Brain Injury Research Center Core GrantP30NS051220 · NINDS · UNIVERSITY OF KENTUCKY · PI HALL, EDWARD D. · 2005 to 2015
$6.4M
Role of calpastatin in modulating function following TBIP01NS058484 · NINDS · UNIVERSITY OF KENTUCKY · PI HALL, EDWARD D. · 2007 to 2011
$4.8M
Preclinical evaluation of IGF1 therapy for traumatic brain injuryR01NS072302 · NINDS · UNIVERSITY OF KENTUCKY · PI SAATMAN, KATHRYN E · 2011 to 2015
$1.8M
NINDS NIH HHS P01 NS058484NINDS NIH HHS P30 NS051220NINDS NIH HHS R01 NS072302
6 · The paper itself

Abstract

Traumatic brain injury (TBI) survivors often suffer from long-lasting cognitive impairment that stems from hippocampal injury. Systemic administration of insulin-like growth factor-1 (IGF-1), a polypeptide growth factor known to play vital roles in neuronal survival, has been shown to attenuate posttraumatic cognitive and motor dysfunction. However, its neuroprotective effects in TBI have not been examined. To this end, moderate or severe contusion brain injury was induced in mice with conditional (postnatal) overexpression of IGF-1 using the controlled cortical impact (CCI) injury model. CCI brain injury produces robust reactive astrocytosis in regions of neuronal damage such as the hippocampus. We exploited this regional astrocytosis by linking expression of hIGF-1 to the astrocyte-specific glial fibrillary acidic protein (GFAP) promoter, effectively targeting IGF-1 delivery to vulnerable neurons. Following brain injury, IGF-1Tg mice exhibited a progressive increase in hippocampal IGF-1 levels which was coupled with enhanced hippocampal reactive astrocytosis and significantly greater GFAP levels relative to WT mice. IGF-1 overexpression stimulated Akt phosphorylation and reduced acute (1 and 3d) hippocampal neurodegeneration, culminating in greater neuron survival at 10d after CCI injury. Hippocampal neuroprotection achieved by IGF-1 overexpression was accompanied by improved motor and cognitive function in brain-injured mice. These data provide strong support for the therapeutic efficacy of increased brain levels of IGF-1 in the setting of TBI.

Indexed as

AnimalsAstrocytesBrain Injuries, TraumaticCognitionDisease Models, AnimalGlial Fibrillary Acidic ProteinGliosisHippocampusHumansInsulin-Like Growth Factor IMemoryMice, TransgenicMotor ActivityNeurodegenerative DiseasesNeuroprotectionPhosphorylationGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseIGF1 protein, humaninsulin-like growth factor-1, mouseInsulin-Like Growth Factor IProto-Oncogene Proteins c-akt

Identifiers

PMID23826235
PMCPMC3695083
OpenAlexW2008437801

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.