Evidence map›Paper›PMID 28233851›Full record

ArticleScientific reports2017

Increased 4R tau expression and behavioural changes in a novel MAPT-N296H genomic mouse model of tauopathy.

Heike J Wobst, Franziska Denk, Peter L Oliver, Achilleas Livieratos, Tonya N Taylor, Maria H Knudsen, Nora Bengoa-Vergniory, David Bannerman, Richard Wade-Martins

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. 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 1 institution in 1 country.

Heike J WobstDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Franziska DenkDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Peter L OliverMRC Functional Genomics Unit, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Achilleas LivieratosMRC Functional Genomics Unit, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Tonya N TaylorDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Maria H KnudsenDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Nora Bengoa-VergnioryDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
David BannermanDepartment of Experimental Psychology, University of Oxford, Oxford, United Kingdom.
Richard Wade-MartinsDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
University of Oxford · GB

Funding

Medical Research Council MR/P007058/1Parkinson's UK H-1102Wellcome TrustWellcome Trust 073141/Z/03/ZWellcome Trust 075406/Z/04/AWellcome Trust 087736/Z/08/ZWellcome Trust 090532/Z/09/Z
6 · The paper itself

Abstract

The microtubule-associated protein tau is implicated in various neurodegenerative diseases including Alzheimer's disease, progressive supranuclear palsy and corticobasal degeneration, which are characterized by intracellular accumulation of hyperphosphorylated tau. Mutations in the tau gene MAPT cause frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17). In the human central nervous system, six tau isoforms are expressed, and imbalances in tau isoform ratios are associated with pathology. To date, few animal models of tauopathy allow for the potential influence of these protein isoforms, relying instead on cDNA-based transgene expression. Using the P1-derived artificial chromosome (PAC) technology, we created mouse lines expressing all six tau isoforms from the human MAPT locus, harbouring either the wild-type sequence or the disease-associated N296H mutation on an endogenous Mapt-/- background. Animals expressing N296H mutant tau recapitulated early key features of tauopathic disease, including a tau isoform imbalance and tau hyperphosphorylation in the absence of somatodendritic tau inclusions. Furthermore, N296H animals displayed behavioural anomalies such as hyperactivity, increased time in the open arms of the elevated plus maze and increased immobility during the tail suspension test. The mouse models described provide an excellent model to study the function of wild-type or mutant tau in a highly physiological setting.

Indexed as

AnimalsAnimals, Genetically ModifiedBehavior, AnimalDisease Models, AnimalGene ExpressionMiceMutant ProteinsProtein IsoformsTauopathiestau ProteinsMAPT protein, humanMutant ProteinsProtein Isoformstau Proteins

Identifiers

PMID28233851
PMCPMC5324134
OpenAlexW2591102555

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.