Evidence map›Paper›PMID 36062141›Full record

ReviewFrontiers in aging neuroscience2022

The prion-like transmission of tau oligomers

Noel A Jackson, Marcos J Guerrero-Muñoz, Diana L Castillo-Carranza

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Neuroinflammation and Tauopathies.Molecular biology reports · 2026
    Review
  6. Review
  7. Article
  8. APOE isoform-associated tau oligomer polymorphs differ in synaptotoxicity and seeding activity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  9. Neuronal Deletion ofBiomolecules · 2025
    Article
  10. Review
  11. Intraneuronal Aβ accumulation causes tau hyperphosphorylation via endolysosomal leakage.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  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.

Noel A JacksonSchool of Public Health, Harvard University, Boston, MA, United States.
Marcos J Guerrero-MuñozSchool of Medicine, University of Monterrey, San Pedro Garza García, Mexico.
Diana L Castillo-CarranzaSchool of Medicine, University of Monterrey, San Pedro Garza García, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The conversion and transmission of misfolded proteins established the basis for the prion concept. Neurodegenerative diseases are considered "prion-like" disorders that lack infectivity. Among them, tauopathies are characterized by the conversion of native tau protein into an abnormally folded aggregate. During the progression of the disease, misfolded tau polymerizes into oligomers and intracellular neurofibrillary tangles (NFTs). While the toxicity of NFTs is an ongoing debate, the contribution of tau oligomers to early onset neurodegenerative pathogenesis is accepted. Tau oligomers are readily transferred from neuron to neuron propagating through the brain inducing neurodegeneration. Recently, transmission of tau oligomers

Indexed as

exosomesmisfoldingprionspreadingtau oligomersvesicles

Identifiers

PMID36062141
PMCPMC9434014

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.