Evidence map›Paper›PMID 24232259›Full record

ArticleExperimental & molecular medicine2013

Amyloid-β oligomers regulate the properties of human neural stem cells through GSK-3β signaling.

Il-Shin Lee, Kwangsoo Jung, Il-Sun Kim, Kook In Park

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

41 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Article
  3. Small-diffusible aggregates, plaques, tangles, and dynamic equilibria: Untangling Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  4. Article
  5. The Hallmarks of Ageing in Microglia.Cellular and molecular neurobiology · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Neurogenesis Is Increased in Human Neural Stem Cells by Aβ40 Peptide.International journal of molecular sciences · 2022
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
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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

4 authors at 2 institutions in 1 country.

Il-Shin LeeDepartment of Pediatrics, Severance Children's Hospital, Yonsei University College of Medicine, Seoul, Korea.
Kwangsoo Jung
Il-Sun Kim
Kook In Park
Yonsei University · KRSeverance Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common cause of age-related dementia. The neuropathological hallmarks of AD include extracellular deposition of amyloid-β peptides and neurofibrillary tangles that lead to intracellular hyperphosphorylated tau in the brain. Soluble amyloid-β oligomers are the primary pathogenic factor leading to cognitive impairment in AD. Neural stem cells (NSCs) are able to self-renew and give rise to multiple neural cell lineages in both developing and adult central nervous systems. To explore the relationship between AD-related pathology and the behaviors of NSCs that enable neuroregeneration, a number of studies have used animal and in vitro models to investigate the role of amyloid-β on NSCs derived from various brain regions at different developmental stages. However, the Aβ effects on NSCs remain poorly understood because of conflicting results. To investigate the effects of amyloid-β oligomers on human NSCs, we established amyloid precursor protein Swedish mutant-expressing cells and identified cell-derived amyloid-β oligomers in the culture media. Human NSCs were isolated from an aborted fetal telencephalon at 13 weeks of gestation and expanded in culture as neurospheres. Human NSCs exposure to cell-derived amyloid-β oligomers decreased dividing potential resulting from senescence through telomere attrition, impaired neurogenesis and promoted gliogenesis, and attenuated mobility. These amyloid-β oligomers modulated the proliferation, differentiation and migration patterns of human NSCs via a glycogen synthase kinase-3β-mediated signaling pathway. These findings contribute to the development of human NSC-based therapy for AD by elucidating the effects of Aβ oligomers on human NSCs.

Indexed as

Amyloid beta-PeptidesAnimalsApoptosisCell MovementCell ProliferationCellular SenescenceCulture Media, ConditionedFetusGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHEK293 CellsHumansMiceMice, Inbred C57BLNeural Stem CellsSignal TransductionAmyloid beta-PeptidesCulture Media, ConditionedGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouse

Identifiers

PMID24232259
PMCPMC3849574
OpenAlexW2018496107

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.