Evidence map›Paper›PMID 23028880›Full record

ArticlePloS one2012

The neuron-astrocyte-microglia triad in normal brain ageing and in a model of neuroinflammation in the rat hippocampus.

Francesca Cerbai, Daniele Lana, Daniele Nosi, Polina Petkova-Kirova, Sandra Zecchi, Holly M Brothers, Gary L Wenk, Maria Grazia Giovannini

Abstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed
–field-weighted citation impact
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

142 citing papers in PubMed.

  1. Article
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  16. Review
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  19. Review
  20. Article

82 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

8 authors.

Francesca CerbaiDepartment of Pharmacology, University of Florence, Florence, Italy.
Daniele Lana
Daniele Nosi
Polina Petkova-Kirova
Sandra Zecchi
Holly M Brothers
Gary L Wenk
Maria Grazia Giovannini

Funding

Vulnerability to neuroinflammation of brainstem ascending aminergic systemsR01AG037320 · NIA · OHIO STATE UNIVERSITY · PI WENK, GARY L. · 2011 to 2015
$1.5M
Aging microglia-neuronal communicationR01AG030331 · NIA · OHIO STATE UNIVERSITY · PI WENK, GARY L. · 2008 to 2012
$1.3M
NIA NIH HHS R01 AG030331NIA NIH HHS R01 AG037320
6 · The paper itself

Abstract

Ageing is accompanied by a decline in cognitive functions; along with a variety of neurobiological changes. The association between inflammation and ageing is based on complex molecular and cellular changes that we are only just beginning to understand. The hippocampus is one of the structures more closely related to electrophysiological, structural and morphological changes during ageing. In the present study we examined the effect of normal ageing and LPS-induced inflammation on astroglia-neuron interaction in the rat hippocampus of adult, normal aged and LPS-treated adult rats. Astrocytes were smaller, with thicker and shorter branches and less numerous in CA1 Str. radiatum of aged rats in comparison to adult and LPS-treated rats. Astrocyte branches infiltrated apoptotic neurons of aged and LPS-treated rats. Cellular debris, which were more numerous in CA1 of aged and LPS-treated rats, could be found apposed to astrocytes processes and were phagocytated by reactive microglia. Reactive microglia were present in the CA1 Str. Radiatum, often in association with apoptotic cells. Significant differences were found in the fraction of reactive microglia which was 40% of total in adult, 33% in aged and 50% in LPS-treated rats. Fractalkine (CX3CL1) increased significantly in hippocampus homogenates of aged and LPS-treated rats. The number of CA1 neurons decreased in aged rats. In the hippocampus of aged and LPS-treated rats astrocytes and microglia may help clearing apoptotic cellular debris possibly through CX3CL1 signalling. Our results indicate that astrocytes and microglia in the hippocampus of aged and LPS-infused rats possibly participate in the clearance of cellular debris associated with programmed cell death. The actions of astrocytes may represent either protective mechanisms to control inflammatory processes and the spread of further cellular damage to neighboring tissue, or they may contribute to neuronal damage in pathological conditions.

Indexed as

AgingAnimalsApoptosisAstrocytesChemokine CX3CL1Disease Models, AnimalHippocampusImmunohistochemistryInflammationLipopolysaccharidesMaleMicrogliaMicroscopy, ConfocalNeuronsPhagocytosisRatsChemokine CX3CL1Lipopolysaccharides

Identifiers

PMID23028880
PMCPMC3445467

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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.