Evidence map›Paper›PMID 25576082›Full record

ArticleNeurobiology of aging2015

Sustained high levels of neuroprotective, high molecular weight, phosphorylated tau in the longest-lived rodent.

Miranda E Orr, Valentina R Garbarino, Angelica Salinas, Rochelle Buffenstein

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Tau Protein Alterations Induced by Hypobaric Hypoxia Exposure.International journal of molecular sciences · 2024
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. DNA Homeostasis and Senescence: Lessons from the Naked Mole Rat.International journal of molecular sciences · 2021
    Review
  8. Perspectives ofAging · 2020
    Article
  9. β-Amyloid aggregation and heterogeneous nucleation.Protein science : a publication of the Protein Society · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
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  19. Article
  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

4 authors at 1 institution in 2 countries.

Miranda E OrrDepartment of Physiology and The Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Valentina R GarbarinoDepartment of Physiology and The Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Angelica SalinasDepartment of Physiology and The Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Rochelle BuffensteinDepartment of Physiology and The Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA. Electronic address: buffenstein@uthscsa.edu.
The University of Texas Health Science Center at San Antonio · US

Funding

TRAINING GRANT ON THE BIOLOGY OF AGINGT32AG021890 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Erzsebet Kokovay, JAMES FLOYD NELSON · 2003 to 2026
$11.4M
Mechanisms of Aging in the Long-lived Naked Mole-RatR01AG022891 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BUFFENSTEIN, ROCHELLE · 2003 to 2007
$1.4M
NIA NIH HHS AG022891NIA NIH HHS R01 AG022891NIA NIH HHS T32 AG021890NIA NIH HHS T32AG021890
6 · The paper itself

Abstract

Tau protein is primarily expressed in neuronal axons and modulates microtubule stability. Tau phosphorylation, aggregation, and subcellular mislocalization coincide with neurodegeneration in numerous diseases, including Alzheimer's disease (AD). During AD pathogenesis, tau misprocessing accompanies Aß accumulation; however, AD animal models, despite elevated Aß, fail to develop tauopathy. To assess whether lack of tau pathology is linked to short life span common to most AD models, we examined tau processing in extraordinarily long-lived, mouse-sized naked mole-rats (NMRs; approximately 32 years), which express appreciable levels of Aß throughout life. We found that NMRs, like other mammals, display highest tau phosphorylation during brain development. Although tau phosphorylation decreases with aging, unexpectedly adult NMRs have higher levels than transgenic mice overexpressing mutant human tau. However, in sharp contrast with the somatodendritic accumulation of misprocessed tau in the transgenic mice, NMRs maintain axonal tau localization. Intriguingly, the adult NMR tau protein is 88 kDa, much larger than 45-68 kDa tau expressed in other mammals. We propose that this 88 kDa tau protein may offer exceptional microtubule stability and neuroprotection against lifelong, elevated Aß.

Indexed as

AgingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAxonsBrainDisease Models, AnimalLongevityMice, TransgenicMolecular WeightMole RatsPhosphorylationTauopathiestau ProteinsAmyloid beta-Peptidestau ProteinsAgingAlzheimer's diseaseAnimal modelNaked mole-ratPhosphorylationTau

Identifiers

PMID25576082
PMCPMC4869521
OpenAlexW2133146732

What OpenQuestion holds

Textmetadata
LicenceTDM
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.