Evidence map›Paper›PMID 29455576›Full record

ArticleJournal of neurotrauma2018

Central Infusion of Insulin-Like Growth Factor-1 Increases Hippocampal Neurogenesis and Improves Neurobehavioral Function after Traumatic Brain Injury.

Shaun W Carlson, Kathryn E Saatman

Abstract read
In one paragraph

Article in Journal of neurotrauma, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Fluconazole Is Neuroprotective via Interactions with the IGF-1 Receptor.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Article
  20. Review
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

2 authors at 1 institution in 1 country.

Shaun W CarlsonSpinal Cord and Brain Injury Research Center, University of Kentucky , Lexington, Kentucky.
Kathryn E SaatmanSpinal Cord and Brain Injury Research Center, University of Kentucky , Lexington, Kentucky.
University of Kentucky · US

Funding

UK Spinal Cord &Brain Injury Research Center Core GrantP30NS051220 · NINDS · UNIVERSITY OF KENTUCKY · PI SULLIVAN, PATRICK G · 2005 to 2015
$6.4M
Preclinical evaluation of IGF1 therapy for traumatic brain injuryR01NS072302 · NINDS · UNIVERSITY OF KENTUCKY · PI SAATMAN, KATHRYN E · 2011 to 2015
$1.8M
Lithium as a Therapeutic Approach to Attenuate Synaptic Deficits after TBIF32NS090748 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CARLSON, SHAUN · 2015 to 2016
$112k
NINDS NIH HHS F32 NS090748NINDS NIH HHS P30 NS051220NINDS NIH HHS R01 NS072302
6 · The paper itself

Abstract

Traumatic brain injury (TBI) produces neuronal dysfunction and cellular loss that can culminate in lasting impairments in cognitive and motor abilities. Therapeutic agents that promote repair and replenish neurons post-TBI hold promise in improving recovery of function. Insulin-like growth factor-1 (IGF-1) is a neurotrophic factor capable of mediating neuroprotective and neuroplasticity mechanisms. Targeted overexpression of IGF-1 enhances the generation of hippocampal newborn neurons in brain-injured mice; however, the translational neurogenic potential of exogenously administered IGF-1 post-TBI remains unknown. In a mouse model of controlled cortical impact, continuous intracerebroventricular infusion of recombinant human IGF-1 (hIGF) for 7 days, beginning 15 min post-injury, resulted in a dose-dependent increase in the number of immature neurons in the hippocampus. Infusion of 10 μg/day of IGF-1 produced detectable levels of hIGF-1 in the cortex and hippocampus and a concomitant increase in protein kinase B activation in the hippocampus. Both motor function and cognition were improved over 7 days post-injury in IGF-1-treated cohorts. Vehicle-treated brain-injured mice showed reduced hippocampal immature neuron density relative to sham controls at 7 days post-injury. In contrast, the density of hippocampal immature neurons in brain-injured mice receiving acute onset IGF-1 infusion was significantly higher than in injured mice receiving vehicle and equivalent to that in sham-injured control mice. Importantly, the neurogenic effect of IGF-1 was maintained with as much as a 6-h delay in the initiation of infusion. These data suggest that central infusion of IGF-1 enhances the generation of immature neurons in the hippocampus, with a therapeutic window of at least 6 h post-injury, and promotes neurobehavioral recovery post-TBI.

Indexed as

AnimalsBrain Injuries, TraumaticHippocampusHumansInfusions, IntraventricularInsulin-Like Growth Factor IMaleMiceMice, Inbred C57BLNeurogenesisRecovery of FunctionIGF1 protein, humanInsulin-Like Growth Factor IcognitionhippocampusIGF-1neurogenesisTBI

Identifiers

PMID29455576
PMCPMC5998830
OpenAlexW2788075153

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.