Evidence map›Paper›PMID 27505014›Full record

ReviewThe Yale journal of biology and medicine2016

Neural stem/progenitor cells in Alzheimer's disease.

Gizem Tincer, Violeta Mashkaryan, Prabesh Bhattarai, Caghan Kizil

Open access · greenAbstract readReview
In one paragraph

Review in The Yale journal of biology and medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Identification and functional characterization of CD133Molecular and cellular biochemistry · 2022
    Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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.

Gizem TincerGerman Centre for Neurodegenerative Diseases (DZNE) Dresden within Helmholtz Association, Arnoldstr. 18, 01307, Dresden, Germany; DFG-Center for Regenerative Therapies Dresden (CRTD), TU Dresden, Fetscherstr. 105, 01307, Dresden, Germany.
Violeta MashkaryanGerman Centre for Neurodegenerative Diseases (DZNE) Dresden within Helmholtz Association, Arnoldstr. 18, 01307, Dresden, Germany; DFG-Center for Regenerative Therapies Dresden (CRTD), TU Dresden, Fetscherstr. 105, 01307, Dresden, Germany.
Prabesh BhattaraiGerman Centre for Neurodegenerative Diseases (DZNE) Dresden within Helmholtz Association, Arnoldstr. 18, 01307, Dresden, Germany; DFG-Center for Regenerative Therapies Dresden (CRTD), TU Dresden, Fetscherstr. 105, 01307, Dresden, Germany.
Caghan KizilGerman Centre for Neurodegenerative Diseases (DZNE) Dresden within Helmholtz Association, Arnoldstr. 18, 01307, Dresden, Germany; DFG-Center for Regenerative Therapies Dresden (CRTD), TU Dresden, Fetscherstr. 105, 01307, Dresden, Germany.
German Center for Neurodegenerative Diseases · DETU Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most prevalent neurodegenerative disease and a worldwide health challenge. Different therapeutic approaches are being developed to reverse or slow the loss of affected neurons. Another plausible therapeutic way that may complement the studies is to increase the survival of existing neurons by mobilizing the existing neural stem/progenitor cells (NSPCs) - i.e. "induce their plasticity" - to regenerate lost neurons despite the existing pathology and unfavorable environment. However, there is controversy about how NSPCs are affected by the unfavorable toxic environment during AD. In this review, we will discuss the use of stem cells in neurodegenerative diseases and in particular how NSPCs affect the AD pathology and how neurodegeneration affects NSPCs. In the end of this review, we will discuss how zebrafish as a useful model organism with extensive regenerative ability in the brain might help to address the molecular programs needed for NSPCs to respond to neurodegeneration by enhanced neurogenesis.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsHumansNeural Stem CellsNeurogenesisPeptide FragmentsZebrafishAmyloid beta-Peptidesamyloid beta-protein (1-42)Peptide FragmentsAlzheimer’s diseaseAmyloid-beta-42humaninduced plasticitymouseneural stem/progenitor cellzebrafish

Identifiers

PMID27505014
PMCPMC4797833
OpenAlexW2413109756

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.