Evidence map›Paper›PMID 30590040›Full record

ArticleCell reports2018

Culling Less Fit Neurons Protects against Amyloid-β-Induced Brain Damage and Cognitive and Motor Decline.

Dina S Coelho, Silvia Schwartz, Marisa M Merino, Barbara Hauert, Barbara Topfel, Colin Tieche, Christa Rhiner, Eduardo Moreno

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Frontiers in neuroscience · 2023
    Review
  15. Azot expression in theCommunicative & integrative biology · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

8 authors at 3 institutions in 2 countries.

Dina S CoelhoCell Fitness Lab, Champalimaud Centre for the Unknown, Av. Brasília, 1400-038 Lisbon, Portugal; Institute for Cell Biology, University of Bern, Baltzerstrasse 4, 3012 Bern, Switzerland.
Silvia SchwartzStem Cells and Regeneration Lab, Champalimaud Centre for the Unknown, Av. Brasília, 1400-038 Lisbon, Portugal.
Marisa M MerinoInstitute for Cell Biology, University of Bern, Baltzerstrasse 4, 3012 Bern, Switzerland; Department of Biochemistry, University of Geneva, Quai Ernest-Ansermet 30, 1211 Geneva 4, Switzerland.
Barbara HauertInstitute for Cell Biology, University of Bern, Baltzerstrasse 4, 3012 Bern, Switzerland.
Barbara TopfelInstitute for Cell Biology, University of Bern, Baltzerstrasse 4, 3012 Bern, Switzerland.
Colin TiecheInstitute for Cell Biology, University of Bern, Baltzerstrasse 4, 3012 Bern, Switzerland.
Christa RhinerInstitute for Cell Biology, University of Bern, Baltzerstrasse 4, 3012 Bern, Switzerland; Stem Cells and Regeneration Lab, Champalimaud Centre for the Unknown, Av. Brasília, 1400-038 Lisbon, Portugal. Electronic address: christa.rhiner@research.fchampalimaud.org.
Eduardo MorenoCell Fitness Lab, Champalimaud Centre for the Unknown, Av. Brasília, 1400-038 Lisbon, Portugal; Institute for Cell Biology, University of Bern, Baltzerstrasse 4, 3012 Bern, Switzerland. Electronic address: eduardo.moreno@research.fchampalimaud.org.
Champalimaud Foundation · PTUniversity of Bern · CHUniversity of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common form of dementia, impairing cognitive and motor functions. One of the pathological hallmarks of AD is neuronal loss, which is not reflected in mouse models of AD. Therefore, the role of neuronal death is still uncertain. Here, we used a Drosophila AD model expressing a secreted form of human amyloid-β42 peptide and showed that it recapitulates key aspects of AD pathology, including neuronal death and impaired long-term memory. We found that neuronal apoptosis is mediated by cell fitness-driven neuronal culling, which selectively eliminates impaired neurons from brain circuits. We demonstrated that removal of less fit neurons delays β-amyloid-induced brain damage and protects against cognitive and motor decline, suggesting that contrary to common knowledge, neuronal death may have a beneficial effect in AD.

Indexed as

Motor ActivityNeuroprotectionAmyloid beta-PeptidesAnimalsBrainCell DeathCognition DisordersCourtshipDisease Models, AnimalDrosophila melanogasterDrosophila ProteinsEpitheliumFemaleHumansHuntington DiseaseLongevityAmyloid beta-Peptidesamyloid beta-protein (1-42)Drosophila ProteinsMutant ProteinsPeptide FragmentsAlzheimer’sapoptosisazotcell competitioncell fitnessDrosophilaneurodegenerationneuronal selectionβ-amyloid

Identifiers

PMID30590040
PMCPMC6315112
OpenAlexW2901466246

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.