Evidence map›Paper›PMID 28671129›Full record

ArticleJournal of Alzheimer's disease : JAD2017

Dual Mechanism of Toxicity for Extracellular Injection of Tau Oligomers versus Monomers in Human Tau Mice.

Giusi Manassero, Michela Guglielmotto, Debora Monteleone, Valeria Vasciaveo, Olena Butenko, Elena Tamagno, Ottavio Arancio, Massimo Tabaton

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Tau Oligomers Neurotoxicity.Life (Basel, Switzerland) · 2021
    Review
  6. The role of wild-type tau in Alzheimer's disease and related tauopathies.Journal of life sciences (Westlake Village, Calif.) · 2020
    Article
  7. Article
  8. Article
  9. The Neurotoxic Role of Extracellular Tau Protein.International journal of molecular sciences · 2018
    Review
  10. 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

8 authors at 4 institutions in 2 countries.

Giusi ManasseroNeuroscience Institute of Cavalieri Ottolenghi Foundation (NICO), University of Torino, Torino, Italy.
Michela GuglielmottoDepartment of Neuroscience, University of Torino, Torino, Italy.
Debora MonteleoneDepartment of Neuroscience, University of Torino, Torino, Italy.
Valeria VasciaveoDepartment of Neuroscience, University of Torino, Torino, Italy.
Olena ButenkoDepartment of Neuroscience, University of Torino, Torino, Italy.
Elena TamagnoDepartment of Neuroscience, University of Torino, Torino, Italy.
Ottavio ArancioDepartment of Pathology and Cell Biology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA.
Massimo TabatonDepartment of Internal Medicine and Medical Specialties (DIMI), Unit of Geriatric Medicine, University of Genova, Genova, Italy.
University of Genoa · ITNeuroscience Institute · ITUniversity of Turin · ITColumbia University · US

Funding

Extracellular tau oligomers and Alzheimer diseaseR01AG049402 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ARANCIO, OTTAVIO · 2015 to 2019
$1.6M
NIA NIH HHS R01 AG049402
6 · The paper itself

Abstract

The mechanism of tau toxicity is still unclear. Here we report that recombinant tau oligomers and monomers, intraventricularly injected in mice with a pure human tau background, foster tau pathology through different mechanisms. Oligomeric forms of tau alter the conformation of tau in a paired helical filament-like manner. This effect occurs without tau hyperphosphorylation as well as activation of specific kinases, suggesting that oligomers of tau induce tau assembly through a nucleation effect. Monomers, in turn, induce neurodegeneration through a calpain-mediated tau cleavage that leads to accumulation of a 17 kDa neurotoxic peptide and induction of apoptotic cell death.

Indexed as

Animalsbcl-2-Associated X ProteinCalpainDisease Models, AnimalExtracellular FluidGreen Fluorescent ProteinsHumansInjections, IntraventricularMiceMice, TransgenicNeurotoxicity SyndromesPhosphorylationProto-Oncogene Proteins c-bcl-2Recombinant ProteinsSignal Transductiontau Proteinsbcl-2-Associated X ProteinCalpainenhanced green fluorescent proteinGreen Fluorescent ProteinsProto-Oncogene Proteins c-bcl-2Recombinant Proteinstau ProteinsAlzheimer’s diseasehTau micepaired helical filamentstau protein

Identifiers

PMID28671129
PMCPMC8957650
OpenAlexW2734302162

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.