Evidence map›Paper›PMID 22885031›Full record

ArticleFree radical biology & medicine2012

Sporadic Alzheimer disease fibroblasts display an oxidative stress phenotype.

Mahesh Ramamoorthy, Peter Sykora, Morten Scheibye-Knudsen, Christopher Dunn, Cindy Kasmer, Yongqing Zhang, Kevin G Becker, Deborah L Croteau, Vilhelm A Bohr

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.5field-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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Liraglutide Protects Against Brain Amyloid-βInternational journal of molecular sciences · 2020
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. NADProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  18. Article
  19. Review
  20. Nutrients, Microglia Aging, and Brain Aging.Oxidative medicine and cellular longevity · 2016
    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

9 authors at 3 institutions in 1 country.

Mahesh RamamoorthyLaboratory of Molecular Gerontology, Biomedical Research Center, 251 Bayview Boulevard, National Institute on Aging, NIH, Baltimore, MD 21224, USA.
Peter Sykora
Morten Scheibye-Knudsen
Christopher Dunn
Cindy Kasmer
Yongqing Zhang
Kevin G Becker
Deborah L Croteau
Vilhelm A Bohr
National Institute on Aging · USInstitute on Aging · USNational Institutes of Health · US

Funding

Analysis of complex biological systems by microarray based gene expressionZICAG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI DE, SUPRIYO · 2009 to 2025
$15.5M
Processing Of Oxidative Stress In AlzheimerZIAAG000735 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$9.4M
Mitochondrial DNA Repair Processes In Oxidative Stress And AgingZIAAG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$9.2M
Oxidative DNA Damage And Its ProcessingZIAAG000727 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$8.4M
OXIDATIVE STRESS MITOCHONDRIAZ01AG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1996 to 2008
$1.6M
Intramural NIH HHS Z01 AG000733Intramural NIH HHS ZIA AG000733NIA NIH HHS Z01-AG000733-14
6 · The paper itself

Abstract

Alzheimer disease (AD) is a major health problem in the United States, affecting one in eight Americans over the age of 65. The number of elderly suffering from AD is expected to continue to increase over the next decade, as the average age of the U.S. population increases. The risk factors for and etiology of AD are not well understood; however, recent studies suggest that exposure to oxidative stress may be a contributing factor. Here, microarray gene expression signatures were compared in AD-patient-derived fibroblasts and normal fibroblasts exposed to hydrogen peroxide or menadione (to simulate conditions of oxidative stress). Using the 23K Illumina cDNA microarray to screen expression of >14,000 human genes, we identified a total of 1017 genes that are chronically up- or downregulated in AD fibroblasts, 215 of which were also differentially expressed in normal human fibroblasts within 12h after exposure to hydrogen peroxide or menadione. Pathway analysis of these 215 genes and their associated pathways revealed cellular functions that may be critically dysregulated by oxidative stress and play a critical role in the etiology and/or pathology of AD. We then examined the AD fibroblasts for the presence of oxidative DNA damage and found increased accumulation of 8-oxo-guanine. These results indicate the possible role of oxidative stress in the gene expression profile seen in AD.

Indexed as

Oxidative StressPhenotypeTranscriptomeAlzheimer DiseaseCase-Control StudiesCells, CulturedDNA DamageFibroblastsGene Expression RegulationHumansHydrogen PeroxideMetabolic Networks and PathwaysOligonucleotide Array Sequence AnalysisOxidantsTranscription, GeneticVitamin K 3Hydrogen PeroxideOxidantsVitamin K 3

Identifiers

PMID22885031
PMCPMC4617209
OpenAlexW2013837108

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.