Evidence map›Paper›PMID 21391234›Full record

ArticleAnnals of neurology2011

Reversible neural stem cell niche dysfunction in a model of multiple sclerosis.

Stine Rasmussen, Jaime Imitola, Angel Ayuso-Sacido, Yue Wang, Sarah C Starossom, Pia Kivisäkk, Bing Zhu, Morten Meyer, Roderick T Bronson, Jose Manuel Garcia-Verdugo and 1 more

Open access · greenAbstract read
In one paragraph

Article in Annals of neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

45 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Frontiers in cellular neuroscience · 2023
    Article
  7. Article
  8. Review
  9. Stem Cells of the Aging Brain.Frontiers in aging neuroscience · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Neuropsychiatric Effects of Antimicrobial Agents.Clinical drug investigation · 2017
    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

11 authors at 5 institutions in 3 countries.

Stine RasmussenCenter for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Jaime Imitola
Angel Ayuso-Sacido
Yue Wang
Sarah C Starossom
Pia Kivisäkk
Bing Zhu
Morten Meyer
Roderick T Bronson
Jose Manuel Garcia-Verdugo
Samia J Khoury
Harvard University · USBrigham and Women's Hospital · USCentro de Investigacion Principe Felipe · ESUniversitat de València · ESUniversity of Southern Denmark · DK

Funding

MHC peptide tetramers in type 1 diabetesU19AI046374 · NIAID · UNIVERSITY OF COLORADO DENVER · PI HOLERS, VERNON MICHAEL · 1999 to 2007
$9.6M
Immune Regulation of Neural Stem Cell Program In EAER01AI043496 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI KHOURY, SAMIA J. · 1999 to 2015
$3.9M
Impact of IFN-gamma on Neural Stem Cell Repair Potential in EAER01AI071448 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI KHOURY, SAMIA J. · 2007 to 2010
$1.4M
NIAID NIH HHS AI043496NIAID NIH HHS AI46374NIAID NIH HHS R01 AI043496NIAID NIH HHS R01 AI071448NIAID NIH HHS U19 AI046374
6 · The paper itself

Abstract

objectiveThe subventricular zone (SVZ) of the brain constitutes a niche for neural stem and progenitor cells that can initiate repair after central nervous system (CNS) injury. In a relapsing-remitting model of experimental autoimmune encephalomyelitis (EAE), the neural stem cells (NSCs) become activated and initiate regeneration during acute disease, but lose this ability during the chronic phases of disease. We hypothesized that chronic microglia activation contributes to the failure of the NSC repair potential in the SVZ.

methodsUsing bromodeoxyuridine injections at different time points during EAE, we quantified the number of proliferating and differentiating progenitors, and evaluated the structure of the SVZ by electron microscopy. In vivo minocycline treatment during EAE was used to address the effect of microglia inactivation on SVZ dysfunction.

resultsIn vivo treatment with minocycline, an inhibitor of microglia activation, increases stem cell proliferation in both naive and EAE animals. Minocycline treatment decreases cortical and periventricular pathology in the chronic phase of EAE, improving the proliferation of Sox2 stem cells and NG2 oligodendrocyte precursors cells originating in the SVZ and their differentiation into mature oligodendrocytes.

interpretationThese data suggest that failure of repair observed during chronic EAE correlates with microglia activation and that treatments targeting chronic microglial activation have the potential for enhancing repair in the CNS.

Indexed as

AnimalsAnti-Bacterial AgentsBromodeoxyuridineCell CountCell MovementCell ProliferationDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalMiceMicrogliaMicroscopy, Electron, TransmissionMinocyclineMultiple SclerosisMyelin Proteolipid ProteinNeural Stem CellsOligodendrogliaAnti-Bacterial AgentsBromodeoxyuridineMinocyclineMyelin Proteolipid Proteinmyelin proteolipid protein (139-151)Peptide Fragments

Identifiers

PMID21391234
PMCPMC3082630
OpenAlexW2047614944

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.