Evidence map›Paper›PMID 26010831›Full record

ReviewGlia2015

Modeling cognition and disease using human glial chimeric mice.

Steven A Goldman, Maiken Nedergaard, Martha S Windrem

Abstract readReview
In one paragraph

Review in Glia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Tracking human neurologic disease status in mouse brain/plasma using reporter-tagged, EV-associated biomarkers.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. The elusive varicose astrocytes.Trends in neurosciences · 2022
    Article
  12. Review
  13. Glial evolution as a determinant of human behavior and its disorders.Annals of the New York Academy of Sciences · 2020
    Review
  14. Article
  15. Uses for humanised mouse models in precision medicine for neurodegenerative disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2019
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

3 authors.

Steven A GoldmanCenter for Translational Neuromedicine, University of Rochester Medical Center, Rochester, New York.
Maiken NedergaardCenter for Translational Neuromedicine, University of Rochester Medical Center, Rochester, New York.
Martha S WindremCenter for Translational Neuromedicine, University of Rochester Medical Center, Rochester, New York.

Funding

A Humanized Mouse Model of Astrocytic Pathology in SchizophreniaR01MH099578 · NIMH · UNIVERSITY OF ROCHESTER · PI GOLDMAN, STEVEN ALAN, NEDERGAARD, MAIKEN · 2013 to 2017
$2.8M
An iPSC based humanized mouse model of dysmyelination in schizophreniaR01MH104701 · NIMH · UNIVERSITY OF ROCHESTER · PI GOLDMAN, STEVEN ALAN · 2014 to 2018
$2.1M
Molecular Regulation of Human Glial Progenitor Cell-Based RemyelinationR01NS075345 · NINDS · UNIVERSITY OF ROCHESTER · PI GOLDMAN, STEVEN ALAN · 2011 to 2015
$1.7M
NIMH NIH HHS R01 MH099578NIMH NIH HHS R01 MH104701NINDS NIH HHS R01 NS075345
6 · The paper itself

Abstract

As new methods for producing and isolating human glial progenitor cells (hGPCs) have been developed, the disorders of myelin have become especially compelling targets for cell-based therapy. Yet as animal modeling of glial progenitor cell-based therapies has progressed, it has become clear that transplanted hGPCs not only engraft and expand within murine hosts, but dynamically outcompete the resident progenitors so as to ultimately dominate the host brain. The engrafted human progenitor cells proceed to generate parenchymal astrocytes, and when faced with a hypomyelinated environment, oligodendrocytes as well. As a result, the recipient brains may become inexorably humanized with regards to their resident glial populations, yielding human glial chimeric mouse brains. These brains provide us a fundamentally new tool by which to assess the species-specific attributes of glia in modulating human cognition and information processing. In addition, the cellular humanization of these brains permits their use in studying glial infectious and inflammatory disorders unique to humans, and the effects of those disorders on the glial contributions to cognition. Perhaps most intriguingly, by pairing our ability to construct human glial chimeras with the production of patient-specific hGPCs derived from pluripotential stem cells, we may now establish mice in which a substantial proportion of resident glia are both human and disease-derived. These mice in particular may provide us new opportunities for studying the human-specific contributions of glia to psychopathology, as well as to higher cognition. As such, the assessment of human glial chimeric mice may provide us new insight into the species-specific contributions of glia to human cognitive evolution, as well as to the pathogenesis of human neurological and neuropsychiatric disease.

Indexed as

AnimalsCentral Nervous System DiseasesChimeraCognitionHumansMiceModels, AnimalNeural Stem CellsNeurogliacell transplantglial progenitormouse modelsneural stem celloligodendrocytic progenitor

Identifiers

PMID26010831
PMCPMC4527525

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.