Evidence map›Paper›PMID 24352739›Full record

ReviewOpen biology2013

Neuron-glia crosstalk in health and disease: fractalkine and CX3CR1 take centre stage.

Graham K Sheridan, Keith J Murphy

Open access · goldAbstract readReview
In one paragraph

Review in Open biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 201 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
201citing papers in PubMed, 1 pooled it
12.5field-weighted citation impact, top 1% 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

201 citing papers in PubMed, 1 synthesis or guideline pooled it, 335 citations in OpenAlex.

  1. Pooled it
  2. The neuroimmune-glutamate hypothesis of addiction.Neuroscience and biobehavioral reviews · 2026
    Review
  3. Article
  4. Article
  5. PPARγ Mediates Transdifferentiation of CX3CR1International journal of molecular sciences · 2026
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Sex-specific dysregulation of the CXProgress in neuro-psychopharmacology & biological psychiatry · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Revisiting the critical roles of reactive microglia in traumatic brain injury.International journal of surgery (London, England) · 2025
    Review
  17. Article
  18. Article
  19. Article
  20. Article

141 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

2 authors at 2 institutions in 2 countries.

Graham K SheridanDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3DY, UK.
Keith J Murphy
University College Dublin · IEUniversity of Cambridge · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An essential aspect of normal brain function is the bidirectional interaction and communication between neurons and neighbouring glial cells. To this end, the brain has evolved ligand-receptor partnerships that facilitate crosstalk between different cell types. The chemokine, fractalkine (FKN), is expressed on neuronal cells, and its receptor, CX(3)CR1, is predominantly expressed on microglia. This review focuses on several important functional roles for FKN/CX(3)CR1 in both health and disease of the central nervous system. It has been posited that FKN is involved in microglial infiltration of the brain during development. Microglia, in turn, are implicated in the developmental synaptic pruning that occurs during brain maturation. The abundance of FKN on mature hippocampal neurons suggests a homeostatic non-inflammatory role in mechanisms of learning and memory. There is substantial evidence describing a role for FKN in hippocampal synaptic plasticity. FKN, on the one hand, appears to prevent excess microglial activation in the absence of injury while promoting activation of microglia and astrocytes during inflammatory episodes. Thus, FKN appears to be neuroprotective in some settings, whereas it contributes to neuronal damage in others. Many progressive neuroinflammatory disorders that are associated with increased microglial activation, such as Alzheimer's disease, show disruption of the FKN/CX(3)CR1 communication system. Thus, targeting CX(3)CR1 receptor hyperactivation with specific antagonists in such neuroinflammatory conditions may eventually lead to novel neurotherapeutics.

Indexed as

AnimalsBrainCentral Nervous System DiseasesChemokine CX3CL1CX3C Chemokine Receptor 1HumansInflammationLearningNeurogliaNeuronal PlasticityNeuronsReceptors, CytokineReceptors, HIVChemokine CX3CL1CX3C Chemokine Receptor 1Receptors, CytokineReceptors, HIVAlzheimer's diseaseCX3CR1fractalkineischaemiamicrogliasynaptic plasticity

Identifiers

PMID24352739
PMCPMC3877844
OpenAlexW2085600478

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.