Evidence map›Paper›PMID 25313506›Full record

ArticleTranslational psychiatry2014

Peripherally triggered and GSK-3β-driven brain inflammation differentially skew adult hippocampal neurogenesis, behavioral pattern separation and microglial activation in response to ibuprofen.

M Llorens-Martín, J Jurado-Arjona, A Fuster-Matanzo, F Hernández, A Rábano, J Ávila

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 67 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

6 authors at 2 institutions in 1 country.

M Llorens-Martín1] Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain [2] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, ISCIII), Madrid, Spain.
J Jurado-Arjona1] Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain [2] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, ISCIII), Madrid, Spain.
A Fuster-Matanzo1] Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain [2] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, ISCIII), Madrid, Spain.
F Hernández1] Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain [2] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, ISCIII), Madrid, Spain.
A Rábano1] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, ISCIII), Madrid, Spain [2] Neuropathology Department, CIEN Foundation, Madrid, Spain.
J Ávila1] Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain [2] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, ISCIII), Madrid, Spain.
Centro de Biología Molecular Severo Ochoa · ESBiomedical Research Networking Center on Neurodegenerative Diseases · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both familial and sporadic forms of Alzheimer disease (AD) present memory impairments. It has been proposed that these impairments are related to inflammation in relevant brain areas such as the hippocampus. Whether peripherally triggered and neuron-driven brain inflammation produce similar and equally reversible alterations is a matter of discussion. Here we studied the effects of ibuprofen administration on a familial AD mouse model overexpressing GSK-3β that presents severe brain inflammation. We compared these effects with those observed in a peripherally triggered brain inflammation model based on chronic lipopolysaccharide (LPS) administration. Both proinflammatory stimuli produced equivalent reversible morphological alterations in granule neurons; however, GSK-3β had a much more prominent role in newborn neuron connectivity, causing alterations that were not reversed by ibuprofen. Although both insults triggered similar behavioral impairments, ibuprofen rescued this defect in LPS-treated mice but did not produce any improvement in GSK-3β-overexpressing animals. This observation could be attributable to the different microglial phenotype induced by ibuprofen treatment. These data may be clinically relevant for AD therapies, as GSK-3β appears to determine the efficacy of ibuprofen treatment.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalBehavior, AnimalDisease Models, AnimalEncephalitisFemaleGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHippocampusIbuprofenMiceMice, Inbred C57BLNeurogenesisNeurogliaAnti-Inflammatory Agents, Non-SteroidalGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseIbuprofen

Identifiers

PMID25313506
PMCPMC4350524
OpenAlexW2025804381

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.