Evidence map›Paper›PMID 24479894›Full record

ArticleActa neuropathologica communications2014

Neuron-to-neuron wild-type Tau protein transfer through a trans-synaptic mechanism: relevance to sporadic tauopathies.

Simon Dujardin, Katia Lécolle, Raphaëlle Caillierez, Séverine Bégard, Nadège Zommer, Cédrick Lachaud, Sébastien Carrier, Noëlle Dufour, Gwennaëlle Aurégan, Joris Winderickx and 4 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed
12.7field-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.

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

142 citing papers in PubMed, 253 citations in OpenAlex.

  1. Article
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82 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

14 authors at 7 institutions in 2 countries.

Simon Dujardin
Katia Lécolle
Raphaëlle Caillierez
Séverine Bégard
Nadège Zommer
Cédrick Lachaud
Sébastien Carrier
Noëlle Dufour
Gwennaëlle Aurégan
Joris Winderickx
Philippe Hantraye
Nicole Déglon
Morvane ColinInserm, UMR837, Place de Verdun, 59045 Lille, France. morvane.colin@inserm.fr.
Luc Buée
Inserm · FRUniversité de Lille · FRCentre National de la Recherche Scientifique · FRCEA Paris-Saclay - Etablissement de Fontenay-aux-roses · FRCentre Hospitalier Universitaire de Lille · FRCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FRKU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn sporadic Tauopathies, neurofibrillary degeneration (NFD) is characterised by the intraneuronal aggregation of wild-type Tau proteins. In the human brain, the hierarchical pathways of this neurodegeneration have been well established in Alzheimer's disease (AD) and other sporadic tauopathies such as argyrophilic grain disorder and progressive supranuclear palsy but the molecular and cellular mechanisms supporting this progression are yet not known. These pathways appear to be associated with the intercellular transmission of pathology, as recently suggested in Tau transgenic mice. However, these conclusions remain ill-defined due to a lack of toxicity data and difficulties associated with the use of mutant Tau.

resultsUsing a lentiviral-mediated rat model of hippocampal NFD, we demonstrated that wild-type human Tau protein is axonally transferred from ventral hippocampus neurons to connected secondary neurons even at distant brain areas such as olfactory and limbic systems indicating a trans-synaptic protein transfer. Using different immunological tools to follow phospho-Tau species, it was clear that Tau pathology generated using mutated Tau remains near the IS whereas it spreads much further using the wild-type one.

conclusionTaken together, these results support a novel mechanism for Tau protein transfer compared to previous reports based on transgenic models with mutant cDNA. It also demonstrates that mutant Tau proteins are not suitable for the development of experimental models helpful to validate therapeutic intervention interfering with Tau spreading.

Indexed as

AnimalsBrainCell DifferentiationCells, CulturedDisease Models, AnimalDisease ProgressionEmbryo, MammalianGene Transfer TechniquesHumansMicrofluidic Analytical TechniquesMicroscopy, ConfocalMicrotubule-Associated ProteinsMutationNeuronsProtein TransportRatsMicrotubule-Associated ProteinsRNA, Messengertau Proteins

Identifiers

PMID24479894
PMCPMC3922636
OpenAlexW2147984390

What OpenQuestion holds

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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.