Evidence map›Paper›PMID 33179866›Full record

ArticleEMBO molecular medicine2020

Fate and propagation of endogenously formed Tau aggregates in neuronal cells.

Patricia Chastagner, Frida Loria, Jessica Y Vargas, Josh Tois, Marc I Diamond, George Okafo, Christel Brou, Chiara Zurzolo

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
  2. Review
  3. Neuroinflammation and Tauopathies.Molecular biology reports · 2026
    Review
  4. Review
  5. Building the bridges: molecular mechanisms of tunneling nanotube formation.Cellular and molecular life sciences : CMLS · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
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  15. Article
  16. Review
  17. Article
  18. Review
  19. Tunneling Nanotubes in the Brain.Results and problems in cell differentiation · 2024
    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

8 authors at 3 institutions in 3 countries.

Patricia ChastagnerUnité de Trafic Membranaire et Pathogenèse, Institut Pasteur, Paris, France.
Frida LoriaUnité de Trafic Membranaire et Pathogenèse, Institut Pasteur, Paris, France.
Jessica Y VargasUnité de Trafic Membranaire et Pathogenèse, Institut Pasteur, Paris, France.
Josh ToisUnité de Trafic Membranaire et Pathogenèse, Institut Pasteur, Paris, France.
Marc I DiamondCenter for Alzheimer's and Neurodegenerative Diseases, Peter O'Donnell Jr. Brain Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
George OkafoGlaxoSmithKline, Stevenage, UK.
Christel BrouUnité de Trafic Membranaire et Pathogenèse, Institut Pasteur, Paris, France.
Chiara ZurzoloUnité de Trafic Membranaire et Pathogenèse, Institut Pasteur, Paris, France.ORCID 0000-0001-6048-6602
Institut Pasteur · FRGlaxoSmithKline (United Kingdom) · GBSouthwestern Medical Center · US

Funding

EU Joint Programme - Neurodegenerative Disease Research (JPND)
6 · The paper itself

Abstract

Tau accumulation in the form of neurofibrillary tangles in the brain is a hallmark of tauopathies such as Alzheimer's disease (AD). Tau aggregates accumulate in brain regions in a defined spatiotemporal pattern and may induce the aggregation of native Tau in a prion-like manner. However, the underlying mechanisms of cell-to-cell spreading of Tau pathology are unknown and could involve encapsulation within exosomes, trans-synaptic passage, and tunneling nanotubes (TNTs). We have established a neuronal cell model to monitor both internalization of externally added fibrils, synthetic (K18) or Tau from AD brain extracts, and real-time conversion of microtubule-binding domain of Tau fused to a fluorescent marker into aggregates. We found that these endogenously formed deposits colabel with ubiquitin and p62 but are not recruited to macroautophagosomes, eventually escaping clearance. Furthermore, endogenous K18-seeded Tau aggregates spread to neighboring cells where they seed new deposits. Transfer of Tau aggregates depends on direct cell contact, and they are found inside TNTs connecting neuronal cells. We further demonstrate that contact-dependent transfer occurs in primary neurons and between neurons and astrocytes in organotypic cultures.

Indexed as

Protein Aggregation, PathologicalAlzheimer DiseaseAnimalsAstrocytesBrainCell LineHumansMiceMice, Inbred C57BLNeurofibrillary TanglesNeuronstau Proteinstau ProteinsautophagyIntercellular spreadingprion-like seedingTau aggregatestunneling nanotubes

Identifiers

PMID33179866
PMCPMC7721367
OpenAlexW3103278178

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.