Evidence map›Paper›PMID 25220759›Full record

ArticleNeurobiology of disease2015

Intracerebral injection of preformed synthetic tau fibrils initiates widespread tauopathy and neuronal loss in the brains of tau transgenic mice.

Eve Peeraer, Astrid Bottelbergs, Kristof Van Kolen, Ilie-Cosmin Stancu, Bruno Vasconcelos, Michel Mahieu, Hilde Duytschaever, Luc Ver Donck, An Torremans, Ellen Sluydts and 8 more

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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

134 citing papers in PubMed, 1 synthesis or guideline pooled it, 210 citations in OpenAlex.

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  19. FGFR3 drives Aβ-induced tau uptake.Experimental & molecular medicine · 2024
    Article
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74 more citing papers are in PubMed but not listed here.

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

18 authors at 5 institutions in 2 countries.

Eve PeeraerDepartment of Neuroscience, Janssen Research and Development, A Division of Janssen Pharmaceutica NV, B-2340 Beerse, Belgium.
Astrid BottelbergsDepartment of Neuroscience, Janssen Research and Development, A Division of Janssen Pharmaceutica NV, B-2340 Beerse, Belgium.
Kristof Van KolenDepartment of Neuroscience, Janssen Research and Development, A Division of Janssen Pharmaceutica NV, B-2340 Beerse, Belgium.
Ilie-Cosmin StancuUCLouvain, Institute of Neuroscience, Group of Cellular and Molecular Neuroscience, B-1200 Woluwe-Saint-Lambert, Belgium.
Bruno VasconcelosUCLouvain, Institute of Neuroscience, Group of Cellular and Molecular Neuroscience, B-1200 Woluwe-Saint-Lambert, Belgium.
Michel MahieuDepartment of Neuroscience, Janssen Research and Development, A Division of Janssen Pharmaceutica NV, B-2340 Beerse, Belgium.
Hilde DuytschaeverDepartment of Neuroscience, Janssen Research and Development, A Division of Janssen Pharmaceutica NV, B-2340 Beerse, Belgium.
Luc Ver DonckDepartment of Neuroscience, Janssen Research and Development, A Division of Janssen Pharmaceutica NV, B-2340 Beerse, Belgium.
An TorremansHistogenex, B-2020 Antwerp, Belgium.
Ellen SluydtsHistogenex, B-2020 Antwerp, Belgium.
Nathalie Van AckerHistogenex, B-2020 Antwerp, Belgium.
John A KempDepartment of Neuroscience, Janssen Research and Development, A Division of Janssen Pharmaceutica NV, B-2340 Beerse, Belgium.
Marc MerckenDepartment of Neuroscience, Janssen Research and Development, A Division of Janssen Pharmaceutica NV, B-2340 Beerse, Belgium.
Kurt R BrundenCenter for Neurodegenerative Disease Research, Institute on Aging, Department of Pathology and Laboratory, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
John Q TrojanowskiCenter for Neurodegenerative Disease Research, Institute on Aging, Department of Pathology and Laboratory, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Ilse DewachterUCLouvain, Institute of Neuroscience, Group of Cellular and Molecular Neuroscience, B-1200 Woluwe-Saint-Lambert, Belgium.
Virginia M Y LeeCenter for Neurodegenerative Disease Research, Institute on Aging, Department of Pathology and Laboratory, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Diederik MoecharsDepartment of Neuroscience, Janssen Research and Development, A Division of Janssen Pharmaceutica NV, B-2340 Beerse, Belgium. Electronic address: dmoechar@its.jnj.com.
Janssen (Belgium) · BEHistoGeneX (Belgium) · BEUCLouvain · BEInstitute 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
NIA NIH HHS P01 AG017586
6 · The paper itself

Abstract

Neurofibrillary tangles composed of hyperphosphorylated fibrillized tau are found in numerous tauopathies including Alzheimer's disease. Increasing evidence suggests that tau pathology can be transmitted from cell-to-cell; however the mechanisms involved in the initiation of tau fibrillization and spreading of disease linked to progression of tau pathology are poorly understood. We show here that intracerebral injections of preformed synthetic tau fibrils into the hippocampus or frontal cortex of young tau transgenic mice expressing mutant human P301L tau induces tau hyperphosphorylation and aggregation around the site of injection, as well as a time-dependent propagation of tau pathology to interconnected brain areas distant from the injection site. Furthermore, we show that the tau pathology as a consequence of injection of tau preformed fibrils into the hippocampus induces selective loss of CA1 neurons. Together, our data confirm previous studies on the seeded induction and the spreading of tau pathology in a different tau transgenic mouse model and reveals neuronal loss associated with seeded tau pathology in tau transgenic mouse brain. These results further validate the utility of the tau seeding model in studying disease transmission, and provide a more complete in vivo tauopathy model with associated neurodegeneration which can be used to investigate the mechanisms involved in tau aggregation and spreading, as well as aid in the search for disease modifying treatments for Alzheimer's disease and related tauopathies.

Indexed as

TauopathiesAge FactorsAnalysis of VarianceAnimalsDisease Models, AnimalDisease ProgressionFunctional LateralityGene Expression RegulationHippocampusHumansMiceMice, TransgenicMutationNeurofibrillary Tanglestau Proteinstau ProteinsCell deathSeedingSpreadingTau pathology

Identifiers

PMID25220759
PMCPMC4303592
OpenAlexW1979363343

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.