Evidence map›Paper›PMID 28978354›Full record

ArticleMolecular neurodegeneration2017

The CNS in inbred transgenic models of 4-repeat Tauopathy develops consistent tau seeding capacity yet focal and diverse patterns of protein deposition.

Ghazaleh Eskandari-Sedighi, Nathalie Daude, Hristina Gapeshina, David W Sanders, Razieh Kamali-Jamil, Jing Yang, Beipei Shi, Holger Wille, Bernardino Ghetti, Marc I Diamond and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Prion-like strain effects in tauopathies.Cell and tissue research · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Quaternary Structure Changes for PrPMolecular neurobiology · 2021
    Article
  12. Article
  13. 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

12 authors at 5 institutions in 2 countries.

Ghazaleh Eskandari-SedighiCentre for Prions and Protein Folding Diseases, University of Alberta, 204 Brain and Aging Research Building, Edmonton, AB, T6G 2M8, Canada.
Nathalie DaudeCentre for Prions and Protein Folding Diseases, University of Alberta, 204 Brain and Aging Research Building, Edmonton, AB, T6G 2M8, Canada.
Hristina GapeshinaCentre for Prions and Protein Folding Diseases, University of Alberta, 204 Brain and Aging Research Building, Edmonton, AB, T6G 2M8, Canada.
David W SandersCenter for Alzheimer's and Neurodegenerative Diseases, UT Southwestern Medical Center, Dallas, USA.
Razieh Kamali-JamilCentre for Prions and Protein Folding Diseases, University of Alberta, 204 Brain and Aging Research Building, Edmonton, AB, T6G 2M8, Canada.
Jing YangCentre for Prions and Protein Folding Diseases, University of Alberta, 204 Brain and Aging Research Building, Edmonton, AB, T6G 2M8, Canada.
Beipei ShiCentre for Prions and Protein Folding Diseases, University of Alberta, 204 Brain and Aging Research Building, Edmonton, AB, T6G 2M8, Canada.
Holger WilleCentre for Prions and Protein Folding Diseases, University of Alberta, 204 Brain and Aging Research Building, Edmonton, AB, T6G 2M8, Canada.
Bernardino GhettiDepartment of Pathology and Laboratory Medicine, Indiana University, Indianapolis, USA.
Marc I DiamondCenter for Alzheimer's and Neurodegenerative Diseases, UT Southwestern Medical Center, Dallas, USA.
Christopher JanusCenter for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, FL, USA.
David WestawayCentre for Prions and Protein Folding Diseases, University of Alberta, 204 Brain and Aging Research Building, Edmonton, AB, T6G 2M8, Canada. david.westaway@ualberta.ca.
University of Alberta · CAIndiana University – Purdue University Indianapolis · USSouthwestern Medical CenterThe University of Texas Southwestern Medical Center · USUniversity of Florida · US

Funding

Research Education ComponentP30AG010133 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SAYKIN, ANDREW J · 1991 to 2020
$37.3M
CIHR PS148962NIA NIH HHS P30 AG010133
6 · The paper itself

Abstract

backgroundMAPT mutations cause neurodegenerative diseases such as frontotemporal dementia but, strikingly, patients with the same mutation may have different clinical phenotypes.

methodsGiven heterogeneities observed in a transgenic (Tg) mouse line expressing low levels of human (2 N, 4R) P301L Tau, we backcrossed founder stocks of mice to C57BL/6Tac, 129/SvEvTac and FVB/NJ inbred backgrounds to discern the role of genetic versus environmental effects on disease-related phenotypes.

resultsThree inbred derivatives of a TgTau

conclusionsQualitative variations in the neuroanatomy of Tau deposition in genetically constrained slow models of primary Tauopathy establish that non-synchronous, focal events contribute to the pathogenic process. Phenotypic diversity in these models suggests a potential parallel to the phenotypic variation seen in P301L patients.

Indexed as

AnimalsBrainDisease Models, AnimalHumansMiceMice, Inbred C57BLMice, TransgenicPhenotypeTauopathiestau ProteinsMAPT protein, humantau ProteinsAgingFocal pathologyNeuronal lossP301L mutationStochastic eventsTransgenic mouse

Identifiers

PMID28978354
PMCPMC5628424
OpenAlexW2763708652

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Registered trials

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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.