Evidence map›Paper›PMID 24604355›Full record

ArticleMolecular neurobiology2014

Loss of prion protein leads to age-dependent behavioral abnormalities and changes in cytoskeletal protein expression.

Matthias Schmitz, Catharina Greis, Philipp Ottis, Christopher J Silva, Walter J Schulz-Schaeffer, Arne Wrede, Katharina Koppe, Bruce Onisko, Jesús R Requena, Nambirajan Govindarajan and 3 more

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Tau Exon 10 Inclusion by PrPInternational journal of molecular sciences · 2021
    Article
  8. Article
  9. PrPFrontiers in molecular neuroscience · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. α-synuclein interacts with PrPNature neuroscience · 2017
    Article
  16. Review
  17. Physiological Functions of the Cellular Prion Protein.Frontiers in molecular biosciences · 2017
    Review
  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

13 authors at 6 institutions in 3 countries.

Matthias SchmitzDepartment of Neurology, University Medical Center Göttingen, Robert-Koch-Straße 40, 37075, Göttingen, Germany, Matthias.Schmitz@med.uni-goettingen.de.
Catharina Greis
Philipp Ottis
Christopher J Silva
Walter J Schulz-Schaeffer
Arne Wrede
Katharina Koppe
Bruce Onisko
Jesús R Requena
Nambirajan Govindarajan
Carsten Korth
Andre Fischer
Inga Zerr
Heinrich Heine University Düsseldorf · DEUniversitätsmedizin Göttingen · DEGerman Center for Neurodegenerative Diseases · DEUniversity of Göttingen · DECenter for Research in Molecular Medicine and Chronic Diseases · ESWestern Regional Research Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cellular prion protein (PrPC) is a highly conserved protein whose exact physiological role remains elusive. In the present study, we investigated age-dependent behavioral abnormalities in PrPC-knockout (Prnp0/0) mice and wild-type (WT) controls. Prnp0/0 mice showed age-dependent behavioral deficits in memory performance, associative learning, basal anxiety, and nest building behavior. Using a hypothesis-free quantitative proteomic investigation, we found that loss of PrPC affected the levels of neurofilament proteins in an age-dependent manner. In order to understand the biochemical basis of these observations, we analyzed the phosphorylation status of neurofilament heavy chain (NF-H). We found a reduction in NF-H phosphorylation in both Prnp0/0 mice and in PrPC-deficient cells. The expression of Fyn and phospho-Fyn, a potential regulator for NF phosphorylation, was associated with PrPC ablation. The number of β-tubulin III-positive neurons in the hippocampus was diminished in Prnp0/0 mice relative to WT mice. These data indicate that PrPC plays an important role in cytoskeletal organization, brain function, and age-related neuroprotection. Our work represents the first direct biochemical link between these proteins and the observed behavioral phenotypes.

Indexed as

Age FactorsAnimalsBehavior, AnimalConditioning, ClassicalCytoskeletal ProteinsCytoskeletonFearLearningMaleMiceMice, KnockoutMotor ActivityNeuronsPhosphorylationProteomicsPrPC ProteinsCytoskeletal ProteinsPrPC Proteins

Identifiers

PMID24604355
OpenAlexW2039168977

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.