Evidence map›Paper›PMID 26731444›Full record

ArticleTranslational psychiatry2016

Absence of IFNγ promotes hippocampal plasticity and enhances cognitive performance.

S Monteiro, F M Ferreira, V Pinto, S Roque, M Morais, D de Sá-Calçada, C Mota, M Correia-Neves, J J Cerqueira

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.

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  20. Pharmaceuticals (Basel, Switzerland) · 2023
    Article

1 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

9 authors at 1 institution in 1 country.

S MonteiroLife and Health Sciences Research Institute, School of Health Sciences, University of Minho, Campus de Gualtar, Braga, Portugal.ORCID http://orcid.org/0000-0002-3037-9635
F M FerreiraLife and Health Sciences Research Institute, School of Health Sciences, University of Minho, Campus de Gualtar, Braga, Portugal.
V PintoLife and Health Sciences Research Institute, School of Health Sciences, University of Minho, Campus de Gualtar, Braga, Portugal.
S RoqueLife and Health Sciences Research Institute, School of Health Sciences, University of Minho, Campus de Gualtar, Braga, Portugal.ORCID http://orcid.org/0000-0002-6512-996X
M MoraisLife and Health Sciences Research Institute, School of Health Sciences, University of Minho, Campus de Gualtar, Braga, Portugal.
D de Sá-CalçadaLife and Health Sciences Research Institute, School of Health Sciences, University of Minho, Campus de Gualtar, Braga, Portugal.
C MotaLife and Health Sciences Research Institute, School of Health Sciences, University of Minho, Campus de Gualtar, Braga, Portugal.
M Correia-NevesLife and Health Sciences Research Institute, School of Health Sciences, University of Minho, Campus de Gualtar, Braga, Portugal.
J J CerqueiraLife and Health Sciences Research Institute, School of Health Sciences, University of Minho, Campus de Gualtar, Braga, Portugal.
University of Minho · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cognitive functioning can be differentially modulated by components of the immune system. Interferon-γ (IFNγ) is a pro-inflammatory cytokine whose production is altered in many conditions displaying some degree of cognitive deficits, although its role in cognitive functioning is still unclear. Here we show that the absence of IFNγ selectively enhances cognitive behaviours in tasks in which the hippocampus is implicated. Moreover, the absence of IFNγ leads to volumetric and cell density changes that are restricted to the dorsal part of the hippocampus. In the dorsal hippocampus, the absence of this pro-inflammatory cytokine leads to an increase in the numbers of newly born neurons in the subgranular zone of the dentate gyrus (DG), an adult neurogenic niche known to support learning and memory, and to an enlargement of the dendritic arborization of DG granule and cornu ammonis (CA)1 pyramidal neurons. Moreover, it also modestly impacts synaptic plasticity, by decreasing the paired-pulse facilitation in the Schaffer collateral to CA1 pyramidal cell synapses. Taken together, our results provide evidence that IFNγ is a negative regulator of hippocampal functioning, as its absence positively impacts on dorsal hippocampus structure, cell density, neuronal morphology and synaptic plasticity. Importantly, these neuroplastic changes are associated with improved performance in learning and memory tasks. Therefore, blockage of the IFNγ signalling may present as promising therapeutic targets for the treatment of inflammation-associated cognitive dysfunction.

Indexed as

Interferon-gammaAnimalsCognitionFemaleHippocampusMaleMiceMice, Inbred C57BLNeuronal PlasticityInterferon-gamma

Identifiers

PMID26731444
PMCPMC5073154
OpenAlexW2228881750

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.