Evidence map›Paper›PMID 24263098›Full record

ArticleCell death & disease2013

Amyloid-β(1-42) oligomer accelerates senescence in adult hippocampal neural stem/progenitor cells via formylpeptide receptor 2.

N He, W-L Jin, K-H Lok, Y Wang, M Yin, Z-J Wang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

87 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Article
  7. Article
  8. Article
  9. Entwined processes in Alzheimer's disease: Brain cellular senescence and Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
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  11. Article
  12. Review
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  17. Near-infrared II theranostic agents for the diagnosis and treatment of Alzheimer's disease.European journal of nuclear medicine and molecular imaging · 2024
    Review
  18. Review
  19. Article
  20. Article

27 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

N He1] School of Pharmacy, Shanghai Jiao Tong University, Shanghai 200240, China [2] Department of Internal Medicine, No. 455 Hospital, Shanghai 200240, China.
W-L Jin
K-H Lok
Y Wang
M Yin
Z-J Wang
Shanghai Jiao Tong University · CNChinese People 's Liberation Army No.455 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The failure of adult hippocampal neurogenesis is increasingly considered as an important factor in the pathological correlates for memory decline in Alzheimer's disease (AD). Loss of adult-born neurons and abnormalities of neural stem/progenitor cells (NSPCs) within the dentate gyrus (DG) of adult hippocampus might contribute to this process. In this study, we showed that amyloid-β(1-42) (Aβ42) oligomer triggers senescent phenotype of NSPCs in vitro. Oligomerized Aβ42 induced the production of senescence-associated biomarkers p16 and senescence-associated β-galactosidase (SA-β-gal) in adult mouse hippocampal NSPCs, as well as inhibited cells proliferation and differentiation. In the DG of amyloid precursor protein/presenilin1 (APP/PS1) transgenic mice, the number of senescent NSPCs was significantly increased and senescence-associated protein p16 was upregulated. Formylpeptide receptor 2 (FPR2), one of Aβ42 functional receptors, may be involved in NSPCs senescence. The FPR2 antagonist WRW4 significantly inhibited NSPCs senescence induced by Aβ42. In addition, the activation of p38 mitogen-activated protein kinase (MAPK) in response to the accumulation of reactive oxygen species (ROS) was involved in NSPCs senescence induced by Aβ42. WRW4 inhibited the accumulation of ROS and the activation of p38 MAPK in NSPCs. Our data suggest that Aβ42 accelerates NSPCs senescence via FPR2-dependent activation of its downstream ROS-p38 MAPK signaling, which limits the function of NSPCs and contributes to failure of neurogenesis. This is the first demonstration of NSPCs senescence response to Aβ42.

Indexed as

Amyloid beta-PeptidesAnimalsCells, CulturedCellular SenescenceHippocampusMaleMiceMice, Inbred C57BLNeural Stem CellsOligopeptidesPeptide FragmentsReactive Oxygen SpeciesReceptors, Formyl PeptideAmyloid beta-Peptidesamyloid beta-protein (1-42)formyl peptide receptor 2, mouseOligopeptidesPeptide FragmentsReactive Oxygen SpeciesReceptors, Formyl Peptidetryptophyl-arginyl-tryptophyl-tryptophyl-tryptophyl-tryptophanamide

Identifiers

PMID24263098
PMCPMC3847315
OpenAlexW1980729492

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.