Evidence map›Paper›PMID 28302722›Full record

ArticleThe Journal of biological chemistry2017

Amyloid-β oligomers transiently inhibit AMP-activated kinase and cause metabolic defects in hippocampal neurons.

Gisele S Seixas da Silva, Helen M Melo, Mychael V Lourenco, Natalia M Lyra E Silva, Marcelo B de Carvalho, Soniza V Alves-Leon, Jorge M de Souza, William L Klein, Wagner S da-Silva, Sergio T Ferreira and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 63 citations in OpenAlex.

  1. Holdfast-Derived Lipid Extract from the Patagonian MacroalgaPharmaceuticals (Basel, Switzerland) · 2026
    Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Inhibition of VDAC1 Rescues AMediators of inflammation · 2023
    Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Alzheimer's disease treatment: The share of herbal medicines.Iranian journal of basic medical sciences · 2021
    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

11 authors at 4 institutions in 3 countries.

Gisele S Seixas da SilvaFrom the Institute of Medical Biochemistry Leopoldo de Meis and.
Helen M MeloFrom the Institute of Medical Biochemistry Leopoldo de Meis and.
Mychael V LourencoFrom the Institute of Medical Biochemistry Leopoldo de Meis and.
Natalia M Lyra E SilvaFrom the Institute of Medical Biochemistry Leopoldo de Meis and.
Marcelo B de CarvalhoFrom the Institute of Medical Biochemistry Leopoldo de Meis and.
Soniza V Alves-Leonthe Divisions of Neurology/Epilepsy Program and.
Jorge M de SouzaNeurosurgery, Clementino Fraga Filho Hospital, Federal University of Rio De Janeiro, Rio de Janeiro 21941-902, Brazil.
William L Kleinthe Department of Neurobiology, Northwestern University, Evanston, Illinois 60208-3520, and.
Wagner S da-SilvaFrom the Institute of Medical Biochemistry Leopoldo de Meis and.
Sergio T FerreiraFrom the Institute of Medical Biochemistry Leopoldo de Meis and.
Fernanda G De FeliceFrom the Institute of Medical Biochemistry Leopoldo de Meis and felice@bioqmed.ufrj.br.
Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro · BRHospital Universitário Clementino Fraga Filho · BRNorthwestern University · USQueen's University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AMP-activated kinase (AMPK) is a key player in energy sensing and metabolic reprogramming under cellular energy restriction. Several studies have linked impaired AMPK function to peripheral metabolic diseases such as diabetes. However, the impact of neurological disorders, such as Alzheimer disease (AD), on AMPK function and downstream effects of altered AMPK activity on neuronal metabolism have been investigated only recently. Here, we report the impact of Aβ oligomers (AβOs), synaptotoxins that accumulate in AD brains, on neuronal AMPK activity. Short-term exposure of cultured rat hippocampal neurons or

Indexed as

Adenosine TriphosphateAlzheimer DiseaseAMP-Activated Protein KinasesAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsGlucose Transport Proteins, FacilitativeHippocampusHumansInsulinNeuronsPeptide FragmentsRatsReceptors, N-Methyl-D-AspartateAdenosine TriphosphateAMP-Activated Protein KinasesAmyloid beta-Peptidesamyloid beta-protein (1-42)Amyloid beta-Protein PrecursorAPP protein, humanGlucose Transport Proteins, FacilitativeInsulinPeptide FragmentsReceptors, N-Methyl-D-AspartateAlzheimer diseaseAMP-activated kinase (AMPK)amyloid-β oligomersATPenergy metabolismGLUTsN-methyl-d-aspartate receptor (NMDA receptor, NMDAR)

Identifiers

PMID28302722
PMCPMC5418041
OpenAlexW2596326857

What OpenQuestion holds

Textmetadata
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.