Evidence map›Paper›PMID 24120836›Full record

ReviewBiochimica et biophysica acta2014

Abeta, oxidative stress in Alzheimer disease: evidence based on proteomics studies.

Aaron M Swomley, Sarah Förster, Jierel T Keeney, Judy Triplett, Zhaoshu Zhang, Rukhsana Sultana, D Allan Butterfield

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
12.2field-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

91 citing papers in PubMed, 186 citations in OpenAlex.

  1. Article
  2. Myeloperoxidase as a therapeutic target for oxidative damage in Alzheimer's disease.Journal of enzyme inhibition and medicinal chemistry · 2025
    Review
  3. Article
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  11. Article
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  13. Redox signaling and metabolism in Alzheimer's disease.Frontiers in aging neuroscience · 2022
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

31 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

7 authors at 2 institutions in 2 countries.

Aaron M SwomleyDepartment of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA; Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA.
Sarah FörsterDepartment of Biochemistry, Institute of Animal Sciences, University of Bonn, Bonn, Germany.
Jierel T KeeneyDepartment of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA; Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA.
Judy TriplettDepartment of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA; Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA.
Zhaoshu ZhangDepartment of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA; Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA.
Rukhsana SultanaDepartment of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA; Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA.
D Allan ButterfieldDepartment of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA; Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA. Electronic address: dabcns@uky.edu.
University of Kentucky · USUniversity of Bonn · DE

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
TROPIC, CHOLINERGIC AND PATHOLOGIC CHANGES IN ALZHEIMER'S DISEASEP01AG005119 · NIA · UNIVERSITY OF KENTUCKY · PI ST CLAIR, DARET K · 1985 to 2012
$15.4M
ROLE OF CALCIUM, CALPAINS, AND CASPASES IN NEURODEGENERATIONP01AG010836 · NIA · UNIVERSITY OF KENTUCKY · PI LANDFIELD, PHILIP W. · 1992 to 2008
$12.4M
NCI NIH HHS P30 CA177558NIA NIH HHS AG-05119NIA NIH HHS P01 AG005119NIA NIH HHS P01 AG010836
6 · The paper itself

Abstract

The initiation and progression of Alzheimer disease (AD) is a complex process not yet fully understood. While many hypotheses have been provided as to the cause of the disease, the exact mechanisms remain elusive and difficult to verify. Proteomic applications in disease models of AD have provided valuable insights into the molecular basis of this disorder, demonstrating that on a protein level, disease progression impacts numerous cellular processes such as energy production, cellular structure, signal transduction, synaptic function, mitochondrial function, cell cycle progression, and proteasome function. Each of these cellular functions contributes to the overall health of the cell, and the dysregulation of one or more could contribute to the pathology and clinical presentation in AD. In this review, foci reside primarily on the amyloid β-peptide (Aβ) induced oxidative stress hypothesis and the proteomic studies that have been conducted by our laboratory and others that contribute to the overall understanding of this devastating neurodegenerative disease.

Indexed as

Oxidative StressProteomicsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAntioxidantsDisease Models, AnimalHumansAmyloid beta-PeptidesAntioxidantsAlzheimer diseaseAmyloid-βMethionine-35Oxidative stressRedox proteomics

Identifiers

PMID24120836
PMCPMC3981962
OpenAlexW2049796821

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.