Evidence map›Paper›PMID 29088998›Full record

ArticleJournal of neurotrauma2018

Post-Injury Administration of Galantamine Reduces Traumatic Brain Injury Pathology and Improves Outcome.

Jing Zhao, Michael J Hylin, Nobuhide Kobori, Kimberly N Hood, Anthony N Moore, Pramod K Dash

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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Review
  3. Bidirectional Interaction Between the Brain and Bone in Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Combined Use of Guanfacine andNeurotrauma reports · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Agonism of the αExperimental neurology · 2021
    Article
  14. Article
  15. Review
  16. αNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Observational
  17. Article
  18. Review
  19. Review
  20. Article
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 1 institution in 1 country.

Jing ZhaoDepartment of Neurobiology and Anatomy, The University of Texas McGovern Medical School , Houston, Texas.
Michael J HylinDepartment of Neurobiology and Anatomy, The University of Texas McGovern Medical School , Houston, Texas.
Nobuhide KoboriDepartment of Neurobiology and Anatomy, The University of Texas McGovern Medical School , Houston, Texas.
Kimberly N HoodDepartment of Neurobiology and Anatomy, The University of Texas McGovern Medical School , Houston, Texas.
Anthony N MooreDepartment of Neurobiology and Anatomy, The University of Texas McGovern Medical School , Houston, Texas.
Pramod K DashDepartment of Neurobiology and Anatomy, The University of Texas McGovern Medical School , Houston, Texas.
The University of Texas Health Science Center · US

Funding

Alpha7 nicotinic acetylcholine receptors and TBI outcomeR01NS088298 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DASH, PRAMOD K · 2015 to 2019
$2.5M
NINDS NIH HHS R01 NS088298
6 · The paper itself

Abstract

Acetylcholine is an excitatory neurotransmitter in the central nervous system that plays a key role in cognitive function, including learning and memory. Previous studies have shown that experimental traumatic brain injury (TBI) reduces cholinergic neurotransmission, decreases evoked release of acetylcholine, and alters cholinergic receptor levels. Galantamine (U.S. Food and Drug Administration approved for the treatment of vascular dementia and Alzheimer's disease) has been shown to inhibit acetylcholinesterase activity and allosterically potentiate nicotinic receptor signaling. We investigated whether acute administration of galantamine can reduce TBI pathology and improve cognitive function tested days after the termination of the drug treatment. Post-injury administration of galantamine was found to decrease TBI-triggered blood-brain barrier (BBB) permeability (tested 24 h post-injury), attenuate the loss of both GABAergic and newborn neurons in the ipsilateral hippocampus, and improve hippocampal function (tested 10 days after termination of the drug treatment). Specifically, significant improvements in the Morris water maze, novel object recognition, and context-specific fear memory tasks were observed in injured animals treated with galantamine. Although messenger RNAs for both M1 (Nos2, TLR4, and IL-12ß) and M2 (Arg1, CCL17, and Mcr1) microglial phenotypes were elevated post-TBI, galantamine treatment did not alter microglial polarization tested 24 h and 6 days post-injury. Taken together, these findings support the further investigation of galantamine as a treatment for TBI.

Indexed as

AnimalsBlood-Brain BarrierBrainBrain Injuries, TraumaticCholinesterase InhibitorsCognitionGalantamineMaleNeuroprotective AgentsRatsRats, Sprague-DawleyRecovery of FunctionCholinesterase InhibitorsGalantamineNeuroprotective Agentsblood–brain barrier permeabilitycholinergic neurotransmissionGABAergic neurodegenerationmemory impairmentsmicroglial polarization

Identifiers

PMID29088998
PMCPMC5784795
OpenAlexW2766428986

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.