Evidence map›Paper›PMID 19717642›Full record

ArticleThe American journal of pathology2009

Overexpression of wild-type murine tau results in progressive tauopathy and neurodegeneration.

Stephanie J Adams, Richard J P Crook, Michael Deture, Suzanne J Randle, Amy E Innes, Xin Z Yu, Wen-Lang Lin, Brittany N Dugger, Melinda McBride, Mike Hutton and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
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  6. Review
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  8. Alzheimer's Disease: Cellular and Pharmacological Aspects.Geriatrics (Basel, Switzerland) · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Towards early detection of neurodegenerative diseases: A gut feeling.Frontiers in cell and developmental biology · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Developmental Pathogenicity of 4-Repeat Human Tau Is Lost with the P301L Mutation in Genetically Matched Tau-Transgenic Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  19. Review
  20. 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 3 institutions in 1 country.

Stephanie J AdamsDepartment of Neuroscience, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, FL 32224, USA. adams.stephanie@mayo.edu
Richard J P Crook
Michael Deture
Suzanne J Randle
Amy E Innes
Xin Z Yu
Wen-Lang Lin
Brittany N Dugger
Melinda McBride
Mike Hutton
Dennis W Dickson
Eileen McGowan
Mayo Clinic in Florida · USJacksonville College · USWinnMed · US

Funding

TRANSGENIC MODELING OF TAUOPATHYP01AG017216 · NIA · MAYO CLINIC JACKSONVILLE · PI DICKSON, DENNIS WILLIAM · 1999 to 2011
$12.0M
Modeling of Mouse and Human Tau InteractionsF32AG027638 · NIA · MAYO CLINIC JACKSONVILLE · PI ADAMS, STEPHANIE J · 2007 to 2009
$176k
NIA NIH HHS AG027638NIA NIH HHS F32 AG027638NIA NIH HHS P01 AG017216
6 · The paper itself

Abstract

Here, we describe the generation and characterization of a novel tau transgenic mouse model (mTau) that overexpresses wild-type murine tau protein by twofold compared with endogenous levels. Transgenic tau expression was driven by a BAC transgene containing the entire wild-type mouse tau locus, including the endogenous promoter and the regulatory elements associated with the tau gene. The mTau model therefore differs from other tau models in that regulation of the genomic mouse transgene mimics that of the endogenous gene, including normal exon splicing regulation. Biochemical data from the mTau mice demonstrated that modest elevation of mouse tau leads to tau hyperphosphorylation at multiple pathologically relevant epitopes and accumulation of sarkosyl-insoluble tau. The mTau mice show a progressive increase in hyperphosphorylated tau pathology with age up to 15 to 18 months, which is accompanied by gliosis and vacuolization. In contrast, older mice show a decrease in tau pathology levels, which may represent hippocampal neuronal loss occurring in this wild-type model. Collectively, these results describe a novel model of tauopathy that develops pathological changes reminiscent of early stage Alzheimer's disease and other related neurodegenerative diseases, achieved without overexpression of a mutant human tau transgene. This model will provide an important tool for understanding the early events leading to the development of tau pathology and a model for analysis of potential therapeutic targets for sporadic tauopathies.

Indexed as

AgingAnimalsAxonsBreedingChromosomes, Artificial, BacterialGene Expression RegulationGenetic VectorsGenomeMiceMice, TransgenicMyelin SheathNerve DegenerationPhosphorylationSolubilityTauopathiestau Proteinstau Proteins

Identifiers

PMID19717642
PMCPMC2751556
OpenAlexW2022083204

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.