Evidence map›Paper›PMID 27639648›Full record

ReviewBiochemical and biophysical research communications2017

Cellular prion protein as a receptor for amyloid-β oligomers in Alzheimer's disease.

Santiago V Salazar, Stephen M Strittmatter

Abstract readReview
In one paragraph

Review in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

43 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Prion Protein: The Molecule of Many Forms and Faces.International journal of molecular sciences · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Fibrinogen Interaction with Astrocyte ICAM-1 and PrPInternational journal of molecular sciences · 2021
    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

2 authors at 1 institution in 1 country.

Santiago V SalazarCellular Neuroscience, Neurodegeneration & Repair, Departments of Neurology and of Neuroscience, Yale University School of Medicine, New Haven, CT, USA; Department of Genetics, Yale University School of Medicine, New Haven, CT, USA.
Stephen M StrittmatterCellular Neuroscience, Neurodegeneration & Repair, Departments of Neurology and of Neuroscience, Yale University School of Medicine, New Haven, CT, USA. Electronic address: Stephen.Strittmatter@yale.edu.
Yale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Skill Development for Diverse Scientific Careers: A New Course Predoctoral Program in Cellular and Molecular BiologyT32GM007223 · NIGMS · YALE UNIVERSITY · PI BASERGA, SUSAN J · 1985 to 2019
$31.0M
Prion Protein in Alzheimer's Disease PathophysiologyR01AG034924 · NIA · YALE UNIVERSITY · PI STEPHEN M STRITTMATTER · 2010 to 2026
$9.6M
Fyn Inhibition by AZD0530 for Alzheimers DiseaseUH3TR000967 · NCATS · YALE UNIVERSITY · PI NYGAARD, HAAKON BERGE, STRITTMATTER, STEPHEN M · 2014 to 2016
$8.5M
Yale Alzheimer Disease Research CenterP50AG047270 · NIA · YALE UNIVERSITY · PI STRITTMATTER, STEPHEN M · 2015 to 2019
$8.3M
Characterizing and Targeting Pyk2 Kinase in Alzheimer’s DiseaseRF1AG053000 · NIA · YALE UNIVERSITY · PI STRITTMATTER, STEPHEN M · 2016 to 2016
$2.1M
NCATS NIH HHS UH3 TR000967NCATS NIH HHS UL1 TR001863NIA NIH HHS P50 AG047270NIA NIH HHS R01 AG034924NIA NIH HHS RF1 AG053000NIGMS NIH HHS T32 GM007223
6 · The paper itself

Abstract

Soluble oligomers of amyloid-beta (Aβo) are implicated by biochemical and genetic evidence as a trigger for Alzheimer's disease (AD) pathophysiology. A key step is Aβo interaction with the neuronal surface to initiate a cascade of altered signal transduction leading to synaptic dysfunction and damage. This review discusses neuronal cell surface molecules with high affinity selectively for oligomeric disease-associated states of Aβ, with a particular focus on the role of cellular prion protein (PrP

Indexed as

Amyloid beta-PeptidesAnimalsHumansMiceProtein BindingPrPC ProteinsSignal TransductionAmyloid beta-PeptidesPrPC ProteinsAlzheimer's diseaseCellular prion protein

Identifiers

PMID27639648
PMCPMC5303667
OpenAlexW2521030228

What OpenQuestion holds

Textmetadata
LicenceTDM
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.