Evidence map›Paper›PMID 24335530›Full record

ArticleJournal of neuropathology and experimental neurology2014

Modulation of hippocampal neuroplasticity by Fas/CD95 regulatory protein 2 (Faim2) in the course of bacterial meningitis.

Simone C Tauber, Kristian Harms, Björn Falkenburger, Joachim Weis, Bernd Sellhaus, Roland Nau, Jörg B Schulz, Arno Reich

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

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  8. Inhibition ofAging · 2020
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  10. B7 homolog 3 aggravates brain injury in a murine model ofExperimental and therapeutic medicine · 2015
    Article
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.

Simone C TauberFrom the Department of Neurology (SCT, BF, JBS, AR), University Hospital and Institute of Neuropathology (JW, BS), Medical Faculty, RWTH Aachen University, Aachen; Department of Neurodegeneration and Restorative Research (KH), Georg-August University, Göttingen; DFG Research Center, Molecular Physiology of the Brain (CMPB), Göttingen; Department of Geriatrics (RN), Evangelisches Krankenhaus Göttingen-Weende, Göttingen, Germany.
Kristian Harms
Björn Falkenburger
Joachim Weis
Bernd Sellhaus
Roland Nau
Jörg B Schulz
Arno Reich
Nanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103 · DEUniversitätsklinikum Aachen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fas-apoptotic inhibitory molecule 2 (Faim2) is a neuron-specific membrane protein and a member of the evolutionary conserved lifeguard apoptosis regulatory gene family. Its neuroprotective effect in acute neurological diseases has been demonstrated in an in vivo model of focal cerebral ischemia. Here we show that Faim2 is physiologically expressed in the human brain with a changing pattern in cases of infectious meningoencephalitis.In Faim2-deficient mice, there was increased caspase-associated hippocampal apoptotic cell death and an increased extracellular signal-regulated kinase pattern during acute bacterial meningitis induced by subarachnoid infection with Streptococcus pneumoniae type 3 strain. However, after rescuing the animals by antibiotic treatment, Faim2 deficiency led to increased hippocampal neurogenesis at 7 weeks after infection. This was associated with improved performance of Faim2-deficient mice compared to wild-type littermates in the Morris water maze, a paradigm for hippocampal spatial learning and memory. Thus, Faim2 deficiency aggravated degenerative processes in the acute phase but induced regenerative processes in the repair phase of a mouse model of pneumococcal meningitis. Hence, time-dependent modulation of neuroplasticity by Faim2 may offer a new therapeutic approach for reducing hippocampal neuronal cell death and improving cognitive deficits after bacterial meningitis.

Indexed as

AgedAged, 80 and overAnimalsApoptosis Regulatory Proteinsfas ReceptorFemaleHippocampusHumansInfantMaleMembrane ProteinsMeningitis, BacterialMiceMice, KnockoutMiddle AgedNeuronal PlasticityApoptosis Regulatory ProteinsFAIM2 protein, humanFAS protein, humanfas ReceptorMembrane Proteins

Identifiers

PMID24335530
PMCPMC3978830
OpenAlexW1971268224

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.