Evidence map›Paper›PMID 23938027›Full record

ArticleMolecular neurodegeneration2013

Autophagy is involved in oligodendroglial precursor-mediated clearance of amyloid peptide.

Wenxia Li, Yifen Tang, Zhiqin Fan, Ya Meng, Guang Yang, Jia Luo, Zun-Ji Ke

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026
    Review
  3. Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Transgenic Mouse Models of Alzheimer's Disease: An Integrative Analysis.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Review
  17. Microglia Impede Oligodendrocyte Generation in Aged Brain.Journal of inflammation research · 2021
    Article
  18. Article
  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

7 authors at 3 institutions in 2 countries.

Wenxia LiKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 200031, China.
Yifen Tang
Zhiqin Fan
Ya Meng
Guang Yang
Jia Luo
Zun-Ji Ke
Chinese Academy of Sciences · CNShanghai Institutes for Biological Sciences · CNUniversity of Kentucky · US

Funding

GSK3BETA, A MEDIATOR OF ETHANOL NEUROTOXICITYR01AA015407 · NIAAA · WEST VIRGINIA UNIVERSITY · PI JIA LUO · 2005 to 2026
$6.2M
NIAAA NIH HHS R01 AA015407
6 · The paper itself

Abstract

backgroundAccumulation of β-amyloid peptides is an important hallmark of Alzheimer's disease (AD). Tremendous efforts have been directed to elucidate the mechanisms of β-amyloid peptides degradation and develop strategies to remove β-amyloid accumulation. In this study, we demonstrated that a subpopulation of oligodendroglial precursor cells, also called NG2 cells, were a new cell type that can clear β-amyloid peptides in the AD transgene mice and in NG2 cell line.

resultsNG2 cells were recruited and clustered around the amyloid plaque in the APPswe/PS1dE9 mice, which is Alzheimer's disease mouse model. In vitro, NG2 cell line and primary NG2 cells engulfed β-amyloid peptides through the mechanisms of endocytosis in a time dependent manner. Endocytosis is divided into pinocytosis and phagocytosis. Aβ(42) internalization by NG2 cells was mediated by actin-dependent macropinocytosis. The presence of β-amyloid peptides stimulated the autophagic pathway in NG2 cells. Once inside the cells, the β-amyloid peptides in NG2 cells were transported to lysosomes and degraded by autophagy.

conclusionsOur findings suggest that NG2 cells are a new cell type that can clear β-amyloid peptides through endocytosis and autophagy.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAutophagyCells, CulturedDisease Models, AnimalFlow CytometryHumansImmunoblottingImmunohistochemistryMaleMiceMice, TransgenicMicroscopy, Electron, TransmissionNeural Stem CellsOligodendrogliaAmyloid beta-PeptidesRNA, Small Interfering

Identifiers

PMID23938027
PMCPMC3751621
OpenAlexW2118254221

What OpenQuestion holds

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LicenceCC BY
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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.