Evidence map›Paper›PMID 23085937›Full record

ReviewJournal of neurology, neurosurgery, and psychiatry2013

Therapeutic strategies for tau mediated neurodegeneration.

Yasumasa Yoshiyama, Virginia M Y Lee, John Q Trojanowski

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Journal of neurology, neurosurgery, and psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02422485 (A 6 Month, Open-Label, Pilot Futility Clinical Trial of Oral Salsalate for Progressive Supranuclear Palsy), which is not on this map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
9.6field-weighted citation impact, top 1% 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.

NCT02422485 phase1completednot on this mapstarted 2015, after this paper: background citation

A 6 Month, Open-Label, Pilot Futility Clinical Trial of Oral Salsalate for Progressive Supranuclear Palsy

TypeinterventionalSponsorAdam BoxerRan2015 to 2019Enrolled10ConditionsProgressive Supranuclear PalsyArmsSalsalate
3 · Its place in the literature

Who cites it

59 citing papers in PubMed, 130 citations in OpenAlex.

  1. Article
  2. Review
  3. Tau Toxicity in Neurodegeneration.Molecular neurobiology · 2022
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Nanoliposomes as a Therapeutic Tool for Alzheimer's Disease.Frontiers in synaptic neuroscience · 2020
    Review
  12. Review
  13. Article
  14. Current and Future Treatments in Alzheimer Disease: An Update.Journal of central nervous system disease · 2020
    Review
  15. Review
  16. Article
  17. Beta-amyloid imaging in dementia.Yeungnam University journal of medicine · 2018
    Review
  18. Article
  19. Review
  20. 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

3 authors at 3 institutions in 2 countries.

Yasumasa YoshiyamaDepartment of Neurology, Chiba East National Hospital, 673 Nitona, Chuo Ward, Chiba, Chiba 260-8712, Japan. neuroyy@cehpnet.com
Virginia M Y Lee
John Q Trojanowski
Chiba Hospital · JPInstitute on Aging · USUniversity of Pennsylvania · US

Funding

Transgenic Mouse Models of Tau PathologiesP01AG017586 · NIA · UNIVERSITY OF PENNSYLVANIA · PI LEE, VIRGINIA M · 2000 to 2021
$37.3M
UPenn ADCC Biomarker CoreP30AG010124 · NIA · UNIVERSITY OF PENNSYLVANIA · PI XIE, SHARON XIANGWEN · 1991 to 2020
$35.1M
NIA NIH HHS P01 AG017586NIA NIH HHS P30 AG010124
6 · The paper itself

Abstract

Based on the amyloid hypothesis, controlling β-amyloid protein (Aβ) accumulation is supposed to suppress downstream pathological events, tau accumulation, neurodegeneration and cognitive decline. However, in recent clinical trials, Aβ removal or reducing Aβ production has shown limited efficacy. Moreover, while active immunisation with Aβ resulted in the clearance of Aβ, it did not prevent tau pathology or neurodegeneration. This prompts the concern that it might be too late to employ Aβ targeting therapies once tau mediated neurodegeneration has occurred. Therefore, it is timely and very important to develop tau directed therapies. The pathomechanisms of tau mediated neurodegeneration are unclear but hyperphosphorylation, oligomerisation, fibrillisation and propagation of tau pathology have been proposed as the likely pathological processes that induce loss of function or gain of toxic function of tau, causing neurodegeneration. Here we review the strategies for tau directed treatments based on recent progress in research on tau and our understanding of the pathomechanisms of tau mediated neurodegeneration.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBiomarkersEnzyme ActivationHumansImmunizationInflammationMicrotubule-Associated ProteinsNeurodegenerative DiseasesNeurofibrillary TanglesPhosphoric Monoester HydrolasesPhosphorylationProtein Processing, Post-TranslationalProteostasis DeficienciesProto-Oncogene Proteins c-fynAmyloid beta-PeptidesBiomarkersMicrotubule-Associated ProteinsPhosphoric Monoester HydrolasesProto-Oncogene Proteins c-fyntau ProteinsAlzheimer's Disease

Identifiers

PMID23085937
PMCPMC3912572
OpenAlexW2112360486

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.