Evidence map›Paper›PMID 36608133›Full record

ArticleScience advances2023

Pathogenic tau-induced transposable element-derived dsRNA drives neuroinflammation.

Elizabeth Ochoa, Paulino Ramirez, Elias Gonzalez, Jasmine De Mange, William J Ray, Kevin F Bieniek, Bess Frost

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
9.4field-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

51 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Riboregulation: a non-canonical tau function.Molecular neurodegeneration · 2026
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

7 authors at 2 institutions in 1 country.

Elizabeth OchoaSam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, TX, USA.ORCID 0000-0002-6765-0951
Paulino RamirezSam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, TX, USA.ORCID 0000-0001-8532-9590
Elias GonzalezSam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, TX, USA.ORCID 0000-0003-1783-5664
Jasmine De MangeSam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, TX, USA.ORCID 0000-0002-1830-207X
William J RayThe Neurodegeneration Consortium, Therapeutics Discovery Division, University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID 0000-0002-4491-167X
Kevin F BieniekGlenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, San Antonio, TX, USA.ORCID 0000-0003-4922-864X
Bess FrostSam and Ann Barshop Institute for Longevity and Aging Studies, San Antonio, TX, USA.ORCID 0000-0002-1212-8138
The University of Texas Health Science Center at San Antonio · USThe University of Texas MD Anderson Cancer Center · US

Funding

South Texas Alzheimer's Disease Research CenterP30AG066546 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Mohamad Habes · 2021 to 2026
$24.0M
Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Recruiting and Retaining URM StudentsR25GM095480 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI OYAJOBI, BABATUNDE OLUKAYODE, WEISS, DAVID S · 2011 to 2021
$3.4M
Investigating the role of transposable element dysregulation as a driver of neurotoxicity in tauopathyRF1NS112391 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI FROST, BESS · 2019 to 2019
$1.9M
NIA NIH HHS P30 AG066546NIGMS NIH HHS R25 GM095480NIH HHS P40 OD018537NINDS NIH HHS RF1 NS112391
6 · The paper itself

Abstract

Deposition of tau protein aggregates in the brain of affected individuals is a defining feature of "tauopathies," including Alzheimer's disease. Studies of human brain tissue and various model systems of tauopathy report that toxic forms of tau negatively affect nuclear and genomic architecture, identifying pathogenic tau-induced heterochromatin decondensation and consequent retrotransposon activation as a causal mediator of neurodegeneration. On the basis of their similarity to retroviruses, retrotransposons drive neuroinflammation via toxic intermediates, including double-stranded RNA (dsRNA). We find that dsRNA and dsRNA sensing machinery are elevated in astrocytes of postmortem brain tissue from patients with Alzheimer's disease and progressive supranuclear palsy and in brains of tau transgenic mice. Using a

Indexed as

Alzheimer DiseaseTauopathiesAdultAnimalsBrainDNA Transposable ElementsDrosophilaHeterochromatinHumansMiceMice, TransgenicNeuroinflammatory DiseasesRetroelementsRNA, Double-Strandedtau ProteinsDNA Transposable ElementsHeterochromatinRetroelementsRNA, Double-Strandedtau Proteins

Identifiers

PMID36608133
PMCPMC9821943
OpenAlexW4313625436

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.