Evidence map›Paper›PMID 22036016›Full record

ReviewCurrent opinion in neurobiology2012

The role of glial cells in synapse elimination.

Won-Suk Chung, Ben A Barres

Abstract readReview
In one paragraph

Review in Current opinion in neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

49 citing papers in PubMed.

  1. Beyond Histamine Blockade: Clemastine Fumarate as a Promoter of Myelin Regeneration, Inflammatory Regulation, and Neuroimmune Modulation in CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  2. Article
  3. Review
  4. Astrocytes Are the Source of TNF Mediating Homeostatic Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. MicroglialThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Small Vessel Disease-Related Dementia: An Invalid Neurovascular Coupling?International journal of molecular sciences · 2020
    Review
  19. Review
  20. 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

2 authors.

Won-Suk ChungDepartment of Neurobiology, Stanford University, School of Medicine, Stanford, CA 94305, USA. wschung@stanford.edu
Ben A Barres

Funding

Does phagocytosis by astrocytes mediate synapse elimination?R21NS072556 · NINDS · STANFORD UNIVERSITY · PI BARRES, BEN A · 2010 to 2011
$443k
NINDS NIH HHS 5 R21NS072556-02NINDS NIH HHS R21 NS072556
6 · The paper itself

Abstract

Excessive synapses generated during early development are eliminated extensively to form functionally mature neural circuits. Synapses in juvenile and mature brains are highly dynamic, and undergo remodeling processes through constant formation and elimination of dendritic spines. Although neural activity has been implicated in initiating the synapse elimination process cell-autonomously, the cellular and molecular mechanisms that transduce changes in correlated neural activity into structural changes in synapses are largely unknown. Recently, however, new findings provide evidence that in different species, glial cells, non-neuronal cell types in the nervous system are crucial in eliminating neural debris and unwanted synapses through phagocytosis. Glial cells not only clear fragmented axons and synaptic debris produced during synapse elimination, but also engulf unwanted synapses thereby actively promoting synapse elimination non-cell autonomously. These new findings support the important role of glial cells in the formation and maintenance of functional neural circuits in development as well as in adult stages and neurodegenerative diseases.

Indexed as

AnimalsBrainCell CommunicationModels, BiologicalNeurogliaNeuronal PlasticityNeuronsSynapses

Identifiers

PMID22036016
PMCPMC3319527

What OpenQuestion holds

Textmetadata
LicenceTDM
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.