Evidence map›Paper›PMID 27802219›Full record

ArticleJournal of Alzheimer's disease : JAD2017

Selenoprotein S Reduces Endoplasmic Reticulum Stress-Induced Phosphorylation of Tau: Potential Role in Selenate Mitigation of Tau Pathology.

Rachel H L H Rueli, Daniel J Torres, Andrea S T Dewing, Arlene C Kiyohara, Stephanie M Barayuga, Miyoko T Bellinger, Jane H Uyehara-Lock, Lon R White, Paula I Moreira, Marla J Berry and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.7field-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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Advances in the treatment of Alzheimer's disease.Frontiers in pharmacology · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. "Alphabet" Selenoproteins: Their Characteristics and Physiological Roles.International journal of molecular sciences · 2023
    Review
  14. CaInternational journal of molecular sciences · 2023
    Article
  15. Selenoprotein S: A versatile disordered protein.Archives of biochemistry and biophysics · 2022
    Review
  16. Diagnosis and Treatment of Alzheimer's Disease:: An Update.Delaware journal of public health · 2021
    Article
  17. Article
  18. Review
  19. Article
  20. Tau-targeting therapies for Alzheimer disease.Nature reviews. Neurology · 2018
    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

12 authors at 4 institutions in 2 countries.

Rachel H L H RueliDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawai'i at Manoa, Honolulu, HI, USA.
Daniel J TorresDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawai'i at Manoa, Honolulu, HI, USA.
Andrea S T DewingDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawai'i at Manoa, Honolulu, HI, USA.
Arlene C KiyoharaDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawai'i at Manoa, Honolulu, HI, USA.
Stephanie M BarayugaDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawai'i at Manoa, Honolulu, HI, USA.
Miyoko T BellingerDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawai'i at Manoa, Honolulu, HI, USA.
Jane H Uyehara-LockDepartment of Pathology, John A. Burns School of Medicine, University of Hawai'i at Manoa, Honolulu, HI, USA.
Lon R WhitePacific Health Research and Education Institute, Honolulu, HI, USA.
Paula I MoreiraCenter for Neuroscience and Cell Biology, University of Coimbra, Coimbra and Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Marla J BerryDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawai'i at Manoa, Honolulu, HI, USA.
George PerryUTSA Neurosciences Institute and Department of Biology, University of Texas at San Antonio, San Antonio, TX, USA.
Frederick P BellingerDepartment of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawai'i at Manoa, Honolulu, HI, USA.
University of Hawaiʻi at Mānoa · USPacific Health Research and Education Institute · USThe University of Texas at San Antonio · USUniversity of Coimbra · PT

Funding

STEERING COMMITTEEU54MD008149 · NIMHD · MOREHOUSE SCHOOL OF MEDICINE · PI OFILI, ELIZABETH O. · 2012 to 2018
$21.1M
RESEARCH DESIGN, BIOSTATISTICS AND RESEARCH ETHICS COREG12MD007601 · NIMHD · UNIVERSITY OF HAWAII AT MANOA · PI BERRY, MARLA J · 2012 to 2016
$13.0M
NIMHD NIH HHS G12 MD007601NIMHD NIH HHS U54 MD008149
6 · The paper itself

Abstract

Previous studies demonstrated that selenium in the form of sodium selenate reduces neurofibrillary tangle formation in Alzheimer's disease models. Hyperphosphorylation of tau, which leads to formation of neurofibrillary tangles in Alzheimer's disease, is increased by endoplasmic reticulum (ER) stress. Selenoprotein S (SelS) is part of an ER membrane complex that removes misfolded proteins from the ER as a means to reduce ER stress. Selenate, as with other forms of selenium, will increase selenoprotein expression. We therefore proposed that increased SelS expression by selenate would contribute to the beneficial actions of selenate in Alzheimer's disease. SelS expression increased with ER stress and decreased under conditions of elevated glucose concentrations in the SH-SY5Y neuronal cell line. Reducing expression of SelS with siRNA promoted cell death in response to ER stress. Selenate increased SelS expression, which significantly correlated with decreased tau phosphorylation. Restricting SelS expression during ER stress conditions increased tau phosphorylation, and also promoted aggregation of phosphorylated tau in neurites and soma. In human postmortem brain, SelS expression coincided with neurofibrillary tangles, but not with amyloid-β plaques. These results indicate that selenate can alter phosphorylation of tau by increasing expression of SelS in Alzheimer's disease and potentially other neurodegenerative disorders.

Indexed as

AgedAged, 80 and overAnalysis of VarianceBrainCell Line, TumorEndoplasmic Reticulum StressGene Expression RegulationGlucoseHumansLeucineMembrane ProteinsMutationNeuroblastomaPhosphorylationProlineRNA, MessengerGlucoseLeucineMembrane ProteinsProlineRNA, MessengerRNA, Small InterferingSelenoproteinsSELENOS protein, humantau ProteinsAlzheimer’s diseaseendoplasmic reticulum stressneurofibrillary tangleseleniumselenoproteintau

Identifiers

PMID27802219
PMCPMC5893862
OpenAlexW2529951006

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.