Evidence map›Paper›PMID 28534873›Full record

ArticleTranslational psychiatry2017

Molecular indicators of stress-induced neuroinflammation in a mouse model simulating features of post-traumatic stress disorder.

S Muhie, A Gautam, N Chakraborty, A Hoke, J Meyerhoff, R Hammamieh, M Jett

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

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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 3 institutions in 1 country.

S MuhieThe Geneva Foundation, Frederick, MD, USA.
A GautamIntegrative Systems Biology, US Army Center for Environmental Health Research, Frederick, MD, USA.
N ChakrabortyThe Geneva Foundation, Frederick, MD, USA.
A HokeThe Geneva Foundation, Frederick, MD, USA.
J MeyerhoffThe Geneva Foundation, Frederick, MD, USA.
R HammamiehIntegrative Systems Biology, US Army Center for Environmental Health Research, Frederick, MD, USA.
M JettIntegrative Systems Biology, US Army Center for Environmental Health Research, Frederick, MD, USA.
Center for Environmental Health · USThe Geneva Foundation · USKennedy Krieger Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A social-stress mouse model was used to simulate features of post-traumatic stress disorder (PTSD). The model involved exposure of an intruder (male C57BL/6) mouse to a resident aggressor (male SJL) mouse for 5 or 10 consecutive days. Transcriptome changes in brain regions (hippocampus, amygdala, medial prefrontal cortex and hemibrain), blood and spleen as well as epigenome changes in the hemibrain were assayed after 1- and 10-day intervals following the 5-day trauma or after 1- and 42-day intervals following the 10-day trauma. Analyses of differentially expressed genes (common among brain, blood and spleen) and differentially methylated promoter regions revealed that neurogenesis and synaptic plasticity pathways were activated during the early responses but were inhibited after the later post-trauma intervals. However, inflammatory pathways were activated throughout the observation periods, except in the amygdala in which they were inhibited only at the later post-trauma intervals. Phenotypically, inhibition of neurogenesis was corroborated by impaired Y-maze behavioral responses. Sustained neuroinflammation appears to drive the development and maintenance of behavioral manifestations of PTSD, potentially via its inhibitory effect on neurogenesis and synaptic plasticity. By contrast, peripheral inflammation seems to be directly responsible for tissue damage underpinning somatic comorbid pathologies. Identification of overlapping, differentially regulated genes and pathways between blood and brain suggests that blood could be a useful and accessible brain surrogate specimen for clinical translation.

Indexed as

AmygdalaAnimalsBehavioral SymptomsBrainDisease Models, AnimalHippocampusInflammationMaleMiceMice, Inbred C57BLNeurogenesisNeuronal PlasticityPrefrontal CortexStress Disorders, Post-TraumaticStress, PsychologicalTranscriptome

Identifiers

PMID28534873
PMCPMC5534959
OpenAlexW2618431211

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.