Evidence map›Paper›PMID 24041015›Full record

ArticleJournal of neurotrauma2014

Reversal of established traumatic brain injury-induced, anxiety-like behavior in rats after delayed, post-injury neuroimmune suppression.

Krista M Rodgers, Yuetiva K Deming, Florencia M Bercum, Serhiy Y Chumachenko, Julie L Wieseler, Kirk W Johnson, Linda R Watkins, Daniel S Barth

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Immunomodulatory and Antioxidant Drugs in Glaucoma Treatment.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  5. Article
  6. Review
  7. Review
  8. Glia and Orofacial Pain: Progress and Future Directions.International journal of molecular sciences · 2021
    Review
  9. Aberrant ER Stress Induced Neuronal-IFNβ Elicits White Matter Injury Due to Microglial Activation and T-Cell Infiltration after TBI.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Chronic neurodegeneration after traumatic brain injury: Alzheimer disease, chronic traumatic encephalopathy, or persistent neuroinflammation?Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
    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

8 authors at 2 institutions in 1 country.

Krista M Rodgers1 Department of Psychology and Neuroscience, University of Colorado , Boulder, Colorado.
Yuetiva K Deming
Florencia M Bercum
Serhiy Y Chumachenko
Julie L Wieseler
Kirk W Johnson
Linda R Watkins
Daniel S Barth
University of Colorado Boulder · USMediciNova (United States) · US

Funding

Preventing Transition of Acute-to-Chronic Neuropathic Pain: Models, Mechanisms &R01DE021966 · NIDCR · UNIVERSITY OF COLORADO · PI BARTH, DANIEL S., FLESHNER, MONIKA · 2011 to 2015
$2.0M
FAST ELECTRICAL OSCILLATIONS IN SOMATOSENSORY CORTEXR01NS036981 · NINDS · UNIVERSITY OF COLORADO AT BOULDER · PI BARTH, DANIEL S. · 1998 to 2006
$1.4M
Immune and Gilia Regulation of Pain & Analgesic ActionsK05DA024044 · NIDA · UNIVERSITY OF COLORADO · PI WATKINS, LINDA · 2008 to 2012
$616k
NIDA NIH HHS DA01767NIDA NIH HHS DA024044NIDCR NIH HHS R01 DE021966NINDS NIH HHS NS36981NINDS NIH HHS R01 NS036981
6 · The paper itself

Abstract

Abstract Traumatic brain injury (TBI) increases the risk of neuropsychiatric disorders, particularly anxiety disorders. Yet, there are presently no therapeutic interventions to prevent the development of post-traumatic anxiety or effective treatments once it has developed. This is because, in large part, of a lack of understanding of the underlying pathophysiology. Recent research suggests that chronic neuroinflammatory responses to injury may play a role in the development of post-traumatic anxiety in rodent models. Acute peri-injury administration of immunosuppressive compounds, such as Ibudilast (MN166), have been shown to prevent reactive gliosis associated with immune responses to injury and also prevent lateral fluid percussion injury (LFPI)-induced anxiety-like behavior in rats. There is evidence in both human and rodent studies that post-traumatic anxiety, once developed, is a chronic, persistent, and drug-refractory condition. In the present study, we sought to determine whether neuroinflammation is associated with the long-term maintenance of post-traumatic anxiety. We examined the efficacy of an anti-inflammatory treatment in decreasing anxiety-like behavior and reactive gliosis when introduced at 1 month after injury. Delayed treatment substantially reduced established LFPI-induced freezing behavior and reactive gliosis in brain regions associated with anxiety and continued neuroprotective effects were evidenced 6 months post-treatment. These results support the conclusion that neuroinflammation may be involved in the development and maintenance of anxiety-like behaviors after TBI.

Indexed as

AnimalsAnxietyBehavior, AnimalBrain InjuriesDisease Models, AnimalFreezing Reaction, CatalepticGliosisImmunosuppressive AgentsIndolizinesMaleMotor ActivityPyrazolesPyridinesRatsTreatment OutcomeibudilastImmunosuppressive AgentsIndolizinesPyrazolesPyridines

Identifiers

PMID24041015
PMCPMC3934516
OpenAlexW2332094297

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.