Evidence map›Paper›PMID 31875547›Full record

ArticleCell reports2019

Dysregulation of RNA Splicing in Tauopathies.

Daniel J Apicco, Cheng Zhang, Brandon Maziuk, Lulu Jiang, Heather I Ballance, Samantha Boudeau, Choong Ung, Hu Li, Benjamin Wolozin

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

62 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
  2. ThebioRxiv : the preprint server for biology · 2026
    Article
  3. Riboregulation: a non-canonical tau function.Molecular neurodegeneration · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. NADScience advances · 2025
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. U1-70K and U1A and tau pathogenesis in demented and non-demented individuals with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Loss of age-associated increase in mbioRxiv : the preprint server for biology · 2025
    Article
  20. Article

2 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

9 authors at 2 institutions in 1 country.

Daniel J ApiccoBoston University School of Medicine, Department of Pharmacology and Experimental Therapeutics, Boston, MA, USA.
Cheng ZhangMayo Clinic, Rochester, MN, USA.
Brandon MaziukBoston University School of Medicine, Department of Pharmacology and Experimental Therapeutics, Boston, MA, USA.
Lulu JiangBoston University School of Medicine, Department of Pharmacology and Experimental Therapeutics, Boston, MA, USA.
Heather I BallanceBoston University School of Medicine, Department of Pharmacology and Experimental Therapeutics, Boston, MA, USA.
Samantha BoudeauBoston University School of Medicine, Department of Pharmacology and Experimental Therapeutics, Boston, MA, USA.
Choong UngMayo Clinic, Rochester, MN, USA.
Hu LiMayo Clinic, Rochester, MN, USA. Electronic address: li.hu@mayo.edu.
Benjamin WolozinBoston University School of Medicine, Department of Pharmacology and Experimental Therapeutics, Boston, MA, USA; Boston University School of Medicine, Department of Neurology, Boston, MA, USA. Electronic address: bwolozin@bu.edu.
Boston University · USMayo Clinic in Arizona · US

Funding

Neuropathology CoreP30AG013846 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KOWALL, NEIL W. · 1996 to 2020
$29.1M
Capturing the molecular complexity of Alzheimer's disease through the lens of RNA binding proteinsRF1AG056318 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LI, HU, WOLOZIN, BENJAMIN L · 2018 to 2020
$4.4M
Stress Granules and the Biology of TDP-43R01ES020395 · NIEHS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WOLOZIN, BENJAMIN L · 2012 to 2016
$4.1M
Systems-level functional proteomics analysis assemblies in Alzheimer's disease and mouse models of tauopathyRF1AG061706 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI EMILI, ANDREW, WOLOZIN, BENJAMIN L · 2019 to 2019
$3.9M
Genetic Modifiers of Protein Interaction Networks in TauopathyR01AG064932 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI EMILI, ANDREW, WOLOZIN, BENJAMIN L · 2019 to 2023
$3.2M
RNA binding proteins as novel targets in Alzheimer's diseaseR01AG050471 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WOLOZIN, BENJAMIN L · 2015 to 2019
$2.9M
The role of acetylation in regulating pathophysiology of tauR01NS089544 · NINDS · MAYO CLINIC JACKSONVILLE · PI PETRUCELLI, LEONARD, WOLOZIN, BENJAMIN L · 2014 to 2018
$1.9M
A network platform to connect drug response and prognosis phenotypes for cancersR01CA196631 · NCI · MAYO CLINIC ROCHESTER · PI LI, HU · 2016 to 2018
$1.2M
Regulation of brain neuroprotection and inflammation by TIA1R21AG059925 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WOLOZIN, BENJAMIN L · 2018 to 2019
$454k
QUANTSTUDIO 12K FLEX OPEN ARRAY REAL-TIME PCR SYSTEMS10OD023663 · OD · BOSTON MEDICAL CENTER · PI DENG, LINGYI L · 2017 to 2017
$186k
NCI NIH HHS R01 CA196631NIA NIH HHS P30 AG013846NIA NIH HHS R01 AG050471NIA NIH HHS R01 AG064932NIA NIH HHS R21 AG059925NIA NIH HHS RF1 AG056318NIA NIH HHS RF1 AG061706NIEHS NIH HHS R01 ES020395NIH HHS S10 OD023663NINDS NIH HHS R01 NS089544
6 · The paper itself

Abstract

Pathological aggregation of RNA binding proteins (RBPs) is associated with dysregulation of RNA splicing in PS19 P301S tau transgenic mice and in Alzheimer's disease brain tissues. The dysregulated splicing particularly affects genes involved in synaptic transmission. The effects of neuroprotective TIA1 reduction on PS19 mice are also examined. TIA1 reduction reduces disease-linked alternative splicing events for the major synaptic mRNA transcripts examined, suggesting that normalization of RBP functions is associated with the neuroprotection. Use of the NetDecoder informatics algorithm identifies key upstream biological targets, including MYC and EGFR, underlying the transcriptional and splicing changes in the protected compared to tauopathy mice. Pharmacological inhibition of MYC and EGFR activity in neuronal cultures tau recapitulates the neuroprotective effects of TIA1 reduction. These results demonstrate that dysfunction of RBPs and RNA splicing processes are major elements of the pathophysiology of tauopathies, as well as potential therapeutic targets for tauopathies.

Indexed as

Alzheimer DiseaseAnimalsBrainDown-RegulationErbB ReceptorsFemaleHeterozygoteHumansMaleMice, Inbred C57BLMice, TransgenicNerve DegenerationNerve Tissue ProteinsProto-Oncogene Proteins c-mycRNA-Binding ProteinsRNA, MessengerErbB ReceptorsNerve Tissue ProteinsProto-Oncogene Proteins c-mycRNA-Binding ProteinsRNA, MessengerT-Cell Intracellular Antigen-1Tia1 protein, mouseEGFRMYCNetDecoderneuroprotectionRNA metabolismRNA-seqRNA splicingstress granuletauopathyTIA1transcriptome

Identifiers

PMID31875547
PMCPMC6941411
OpenAlexW2998410347

What OpenQuestion holds

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Registered trials

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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.