Evidence map›Paper›PMID 24252176›Full record

ArticleActa neuropathologica communications2013

Decreased neuroinflammation and increased brain energy homeostasis following environmental enrichment after mild traumatic brain injury is associated with improvement in cognitive function.

Teresita L Briones, Julie Woods, Magdalena Rogozinska

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Acta neuropathologica communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.6field-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

34 citing papers in PubMed, 58 citations in OpenAlex.

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  12. Exercising New Neurons to Vanquish Alzheimer Disease.Brain plasticity (Amsterdam, Netherlands) · 2018
    Review
  13. Article
  14. Hypertonic Saline Alleviates Brain Edema After Traumatic Brain Injury via Downregulation of Aquaporin 4 in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  15. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Teresita L BrionesDepartment of Adult Health, Cohn Bldg, Rm 344, Wayne State University, 5557 Cass Avenue, Detroit, MI 48202, USA. tbriones@wayne.edu.
Julie Woods
Magdalena Rogozinska
University of Illinois Chicago · USWayne State University · US

Funding

GENE EXPRESSION-ENVIRONMENT LINK IN CEREBRAL ISCHEMIAR01NR007666 · NINR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BRIONES, TERESITA L · 2002 to 2006
$1.4M
NINR NIH HHS R01 NR007666
6 · The paper itself

Abstract

backgroundPersistent neuroinflammation and disruptions in brain energy metabolism is commonly seen in traumatic brain injury (TBI). Because of the lack of success of most TBI interventions and the documented benefits of environmental enrichment (EE) in enhancing brain plasticity, here we focused our study on use of EE in regulating injury-induced neuroinflammation and disruptions in energy metabolism in the prefrontal cortex and hippocampus. Adult male Wistar rats were used in the study and randomly assigned to receive either: mild TBI (mTBI) using the controlled cortical injury model or sham surgery. Following surgery, rats from each group were further randomized to either: EE housing or standard laboratory housing (CON). After 4 weeks of recovery, cognitive testing was performed using the non-matching-to-sample and delayed non-matching-to-sample tasks. After completion of behavioral testing, levels of the pro-inflammatory cytokines IL-1β and TNF-α and the anti-inflammatory cytokine IL-10 were measured. In addition, levels of AMPK (adenosine monophosphate-activated protein kinase), phosphorylated AMPK and uMtCK (ubiquitous mitochondrial creatine kinase) were assessed as measures of brain energy homeostasis.

resultsOur results showed that EE: (1) decreased the pro-inflammatory cytokines IL-1β and TNF-α and enhanced levels of the anti-inflammatory cytokine IL-10 after mTBI; (2) mitigated mTBI-induced cognitive impairment; and (3) attenuated mTBI-induced downregulation in pAMPK/AMPK ratio and uMtCK levels.

conclusionsOur data demonstrated the potential of EE to modulate the persistent: (1) neuroinflammatory response seen following mTBI, and (2) persistent disturbance in brain energy homeostasis. It is possible that through the mechanism of modulating neuroinflammation, EE housing was able to restore the disruption in energy metabolism and enhanced functional recovery after mTBI.

Indexed as

Housing, AnimalAMP-Activated Protein KinasesAnimalsBrain InjuriesCognition DisordersCreatine Kinase, Mitochondrial FormDisease Models, AnimalEnvironmentHippocampusHomeostasisMaleNeuroimmunomodulationPhosphorylationPrefrontal CortexRandom AllocationRats, WistarAMP-Activated Protein KinasesCreatine Kinase, Mitochondrial Form

Identifiers

PMID24252176
PMCPMC3893439
OpenAlexW2105670925

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.