Evidence map›Paper›PMID 31034749›Full record

ReviewThe FEBS journal2019

Tau tubulin kinases in proteinopathy.

Laura M Taylor, Pamela J McMillan, Brian C Kraemer, Nicole F Liachko

Open access · bronzeAbstract readReview
In one paragraph

Review in The FEBS journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Unraveling Molecular Targets for Neurodegenerative Diseases ThroughInternational journal of molecular sciences · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
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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

4 authors at 2 institutions in 1 country.

Laura M TaylorDivision of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington, Seattle, WA, USA.
Pamela J McMillanDepartment of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington, USA.
Brian C KraemerDivision of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington, Seattle, WA, USA.ORCID 0000-0002-2252-7634
Nicole F LiachkoDivision of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington, Seattle, WA, USA.
University of Puget Sound · USUniversity of Washington · US

Funding

GENETIC APPROACHES TO AGING RESEARCHT32AG000057 · NIA · UNIVERSITY OF WASHINGTON · PI RABINOVITCH, PETER S · 1985 to 2019
$14.2M
Developing Neuroprotective Strategies for Tau and TDP-43 Proteinopathy in FTLDR01NS064131 · NINDS · SEATTLE INST FOR BIOMEDICAL/CLINICAL RES · PI KRAEMER, BRIAN C. · 2009 to 2022
$5.0M
Identifying new tau targeted therapeutics: a drug repurposing approachI01BX002619 · VA · VA PUGET SOUND HEALTHCARE SYSTEM · PI KRAEMER, BRIAN C. · 2015 to 2018
–
Inhibiting pathological TDP-43 phosphorylation as a therapeutic strategy for ALSI01BX003755 · VA · VA PUGET SOUND HEALTHCARE SYSTEM · PI KRAEMER, BRIAN C. · 2017 to 2020
–
Investigating calcineurin regulation of pathological TDP-43 phosphorylation in ALSI01BX004044 · VA · VA PUGET SOUND HEALTHCARE SYSTEM · PI LIACHKO, NICOLE FARON · 2019 to 2022
–
BLRD VA I01 BX002619BLRD VA I01 BX003755BLRD VA I01 BX004044NIA NIH HHS T32 AG000057NINDS NIH HHS R01 NS064131
6 · The paper itself

Abstract

A number of neurodegenerative diseases are characterized by deposition of abnormally phosphorylated tau or TDP-43 in disease-affected neurons. These diseases include Alzheimer's disease, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis. No disease-modifying therapeutics is available to treat these disorders, and we have a limited understanding of the cellular and molecular factors integral to disease initiation or progression. Phosphorylated tau and TDP-43 are important markers of pathology in dementia disorders and directly contribute to tau- and TDP-43-related neurotoxicity and neurodegeneration. Here, we review the scope of tau and TDP-43 phosphorylation in neurodegenerative disease and discuss recent work demonstrating the kinases TTBK1 and TTBK2 phosphorylate both tau and TDP-43, promoting neurodegeneration.

Indexed as

AnimalsBrainHumansProtein Serine-Threonine KinasesTDP-43 ProteinopathiesProtein Serine-Threonine Kinasestau-tubulin kinaseALSAlzheimer's diseaseCBDFTLDphosphorylationPick's diseasePSPtautauopathyTDP-43TTBK1TTBK2

Identifiers

PMID31034749
PMCPMC6936727
OpenAlexW2942595531

What OpenQuestion holds

Textmetadata
LicenceTDM
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.