Evidence map›Paper›PMID 25752338›Full record

ReviewAnnals of the New York Academy of Sciences2015

Glia: guardians, gluttons, or guides for the maintenance of neuronal connectivity?

Joseph Jebelli, Wei Su, Stephanie Hopkins, Jennifer Pocock, Gwenn A Garden

Abstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Neuron-Glial Interactions: Implications for Plasticity, Behavior, and Cognition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Review
  2. Article
  3. Article
  4. A Subpopulation of Microglia Generated in the Adult Mouse Brain Originates from Prominin-1-Expressing Progenitors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  5. The Danaid Theory of Aging.Frontiers in cell and developmental biology · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Is Alzheimer's Also a Stem Cell Disease? - The Zebrafish Perspective.Frontiers in cell and developmental biology · 2018
    Article
  11. Article
  12. Review
  13. Inflammation, Glutamate, and Glia: A Trio of Trouble in Mood Disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
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

5 authors.

Joseph JebelliDepartment of Neurology, University of Washington, Seattle, Washington.
Wei SuDepartment of Neurology, University of Washington, Seattle, Washington.
Stephanie HopkinsDepartment of Neurology, University of Washington, Seattle, Washington.
Jennifer PocockDepartment of Neuroinflammation, University College London Institute of Neurology, London, United Kingdom.
Gwenn A GardenDepartment of Neurology, University of Washington, Seattle, Washington.

Funding

Molecular Regulation of Microglia BehaviorR01NS073848 · NINDS · UNIVERSITY OF WASHINGTON · PI GARDEN, GWENN A · 2011 to 2016
$1.7M
RNA Dysfunction in Selectively Vulnerable Populations in SCA7 MiceR21NS086094 · NINDS · UNIVERSITY OF WASHINGTON · PI GARDEN, GWENN A · 2013 to 2014
$431k
NINDS NIH HHS R01 NS073848NINDS NIH HHS R21 NS086094
6 · The paper itself

Abstract

An emerging aspect of neuronal-glial interactions is the connection glial cells have to synapses. Mounting research now suggests a far more intimate relationship than previously recognized. Moreover, the current evidence implicating synapse loss in neurodegenerative disease etiology is overwhelming, but the role of glia in the process of synaptic degeneration has only recently been considered in earnest. Each main class of glial cell, including astrocytes, oligodendrocytes, and microglia, performs crucial and multifaceted roles in the maintenance of synaptic function and excitability. As such, aging and/or neuronal stress from disease-related misfolded proteins may involve disruption of multiple non-cell-autonomous synaptic support systems that are mediated by neighboring glia. In addition, glial cell activation induced by injury, ischemia, or neurodegeneration is thought to greatly alter the behavior of glial cells toward neuronal synapses, suggesting that neuroinflammation potentially contributes to synapse loss primarily mediated by altered glial functions. This review discusses recent evidence highlighting novel roles for glial cells at neuronal synapses and in the maintenance of neuronal connectivity, focusing primarily on their implications for neurodegenerative disease research.

Indexed as

AstrocytesCell CommunicationHumansInflammationMicrogliaMyelin SheathNeurodegenerative DiseasesNeuronsOligodendrogliaSynapsesSynaptic Transmissionglianeurodegenerationsynapse

Identifiers

PMID25752338
PMCPMC4564356

What OpenQuestion holds

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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.