Evidence map›Paper›PMID 21858230›Full record

ArticlePloS one2011

Implicating calpain in tau-mediated toxicity in vivo.

James B Reinecke, Sarah L DeVos, James P McGrath, Amanda M Shepard, Dustin K Goncharoff, Don N Tait, Samantha R Fleming, Michael P Vincent, Michelle L Steinhilb

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

36 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Non-Rodent Genetic Animal Models for Studying Tauopathy: Review ofInternational journal of molecular sciences · 2021
    Review
  8. Review
  9. Article
  10. Review
  11. Neuronal Mitochondria Modulation of LPS-Induced Neuroinflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  12. Review
  13. Article
  14. Calcium-Activated Calpain Specifically Cleaves Glutamate Receptor IIA But Not IIB at theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  15. Review
  16. Article
  17. Article
  18. TauNeuroscience · 2017
    Article
  19. Therapeutic strategies for the treatment of tauopathies: Hopes and challenges.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2016
    Review
  20. The Neurotoxic TAUMolecular medicine (Cambridge, Mass.) · 2016
    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

9 authors at 2 institutions in 1 country.

James B ReineckeDepartment of Biology, Central Michigan University, Mount Pleasant, Michigan, United States of America.
Sarah L DeVos
James P McGrath
Amanda M Shepard
Dustin K Goncharoff
Don N Tait
Samantha R Fleming
Michael P Vincent
Michelle L Steinhilb
Central Michigan University · USMichigan United · US

Funding

Examining Tau Proteolysis in Neurodegenerative DiseaseR15AG032105 · NIA · CENTRAL MICHIGAN UNIVERSITY · PI STEINHILB, MICHELLE L. · 2008 to 2008
$170k
NIA NIH HHS 1 R15 AG032105-01NIA NIH HHS R15 AG032105
6 · The paper itself

Abstract

Alzheimer's disease and other related neurodegenerative disorders known as tauopathies are characterized by the accumulation of abnormally phosphorylated and aggregated forms of the microtubule-associated protein tau. Several laboratories have identified a 17 kD proteolytic fragment of tau in degenerating neurons and in numerous cell culture models that is generated by calpain cleavage and speculated to contribute to tau toxicity. In the current study, we employed a Drosophila tauopathy model to investigate the importance of calpain-mediated tau proteolysis in contributing to tau neurotoxicity in an animal model of human neurodegenerative disease. We found that mutations that disrupted endogenous calpainA or calpainB activity in transgenic flies suppressed tau toxicity. Expression of a calpain-resistant form of tau in Drosophila revealed that mutating the putative calpain cleavage sites that produce the 17 kD fragment was sufficient to abrogate tau toxicity in vivo. Furthermore, we found significant toxicity in the fly retina associated with expression of only the 17 kD tau fragment. Collectively, our data implicate calpain-mediated proteolysis of tau as an important pathway mediating tau neurotoxicity in vivo.

Indexed as

Disease Models, AnimalAnimalsAnimals, Genetically ModifiedBlotting, WesternCalpainCells, CulturedDrosophila ProteinsEyeMicroscopy, Electron, ScanningMutationNeurodegenerative DiseasesNeuronsTauopathiestau ProteinsCalpaincalpain A, DrosophilaCalpB protein, DrosophilaDrosophila Proteinstau Proteins

Identifiers

PMID21858230
PMCPMC3157467
OpenAlexW2000608506

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.