Evidence map›Paper›PMID 24476502›Full record

ArticleJournal of neurotrauma2014

PARP-1 inhibition attenuates neuronal loss, microglia activation and neurological deficits after traumatic brain injury.

Bogdan A Stoica, David J Loane, Zaorui Zhao, Shruti V Kabadi, Marie Hanscom, Kimberly R Byrnes, Alan I Faden

Abstract read
In one paragraph

Article in Journal of neurotrauma, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

62 citing papers in PubMed, 116 citations in OpenAlex.

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  13. Nicotinamide Adenine Dinucleotide (NADAntioxidants & redox signaling · 2023
    Review
  14. Application of P7C3 Compounds to Investigating and Treating Acute and Chronic Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  15. Olaparib Attenuates Demyelination and Neuroinflammation in an Organotypic Slice Culture Model of Metachromatic Leukodystrophy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  16. Review
  17. Article
  18. Article
  19. Epigenetic Modulation of Opioid Receptors by Drugs of Abuse.International journal of molecular sciences · 2022
    Review
  20. Article

2 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

7 authors at 1 institution in 1 country.

Bogdan A Stoica1 Department of Anesthesiology, Center for Shock, Trauma and Anesthesiology Research (STAR), National Study Center for Trauma and EMS, University of Maryland , School of Medicine, Baltimore, Maryland.
David J Loane
Zaorui Zhao
Shruti V Kabadi
Marie Hanscom
Kimberly R Byrnes
Alan I Faden
Uniformed Services University of the Health Sciences · US

Funding

Mechanisms and Modulation of Cell Death in Traumatic Brain InjuryR01NS061839 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI FADEN, ALAN IRA · 2009 to 2012
$1.9M
NINDS NIH HHS R01 NS061839
6 · The paper itself

Abstract

Traumatic brain injury (TBI) causes neuronal cell death as well as microglial activation and related neurotoxicity that contribute to subsequent neurological dysfunction. Poly (ADP-ribose) polymerase (PARP-1) induces neuronal cell death through activation of caspase-independent mechanisms, including release of apoptosis inducing factor (AIF), and microglial activation. Administration of PJ34, a selective PARP-1 inhibitor, reduced cell death of primary cortical neurons exposed to N-Methyl-N'-Nitro-N-Nitrosoguanidine (MNNG), a potent inducer of AIF-dependent cell death. PJ34 also attenuated lipopolysaccharide and interferon-γ-induced activation of BV2 or primary microglia, limiting NF-κB activity and iNOS expression as well as decreasing generation of reactive oxygen species and TNFα. Systemic administration of PJ34 starting as late as 24 h after controlled cortical impact resulted in improved motor function recovery in mice with TBI. Stereological analysis demonstrated that PJ34 treatment reduced the lesion volume, attenuated neuronal cell loss in the cortex and thalamus, and reduced microglial activation in the TBI cortex. PJ34 treatment did not improve cognitive performance in a Morris water maze test or reduce neuronal cell loss in the hippocampus. Overall, our data indicate that PJ34 has a significant, albeit selective, neuroprotective effect after experimental TBI, and its therapeutic effect may be from multipotential actions on neuronal cell death and neuroinflammatory pathways.

Indexed as

Poly(ADP-ribose) Polymerase InhibitorsAnimalsBlotting, WesternBrain InjuriesCell DeathDisease Models, AnimalEnzyme InhibitorsMaleMiceMice, Inbred C57BLMicrogliaNeuronsNeuroprotective AgentsPhenanthrenesPoly (ADP-Ribose) Polymerase-1RatsEnzyme InhibitorsNeuroprotective AgentsN-(oxo-5,6-dihydrophenanthridin-2-yl)-N,N-dimethylacetamide hydrochlorideParp1 protein, mousePhenanthrenesPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase Inhibitors

Identifiers

PMID24476502
PMCPMC3967421
OpenAlexW2319228377

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.