Evidence map›Paper›PMID 30068908›Full record

ArticleScientific reports2018

Evidence supporting oxidative stress in a moderately affected area of the brain in Alzheimer's disease.

Priscilla Youssef, Belal Chami, Julia Lim, Terry Middleton, Greg T Sutherland, Paul K Witting

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Effects of 12 WeeksNutrients · 2021
    Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. In defence of ferroptosis.Signal transduction and targeted therapy · 2025
    Review
  17. Review
  18. Role of NRF2 in Pathogenesis of Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2024
    Review
  19. Review
  20. Article
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

6 authors at 1 institution in 1 country.

Priscilla YoussefRedox Biology Group, Discipline of Pathology, University of Sydney, Sydney, NSW, 2006, Australia.
Belal ChamiRedox Biology Group, Discipline of Pathology, University of Sydney, Sydney, NSW, 2006, Australia.
Julia LimNeuropathology Group, Discipline of Pathology, The University of Sydney, Sydney, NSW, 2006, Australia.
Terry MiddletonNeuropathology Group, Discipline of Pathology, The University of Sydney, Sydney, NSW, 2006, Australia.
Greg T SutherlandNeuropathology Group, Discipline of Pathology, The University of Sydney, Sydney, NSW, 2006, Australia.
Paul K WittingRedox Biology Group, Discipline of Pathology, University of Sydney, Sydney, NSW, 2006, Australia. paul.witting@sydney.edu.au.ORCID 0000-0003-2237-7004
The University of Sydney · AU

Funding

Brain Tissue Resource Centre for Alcohol ResearchR28AA012725 · NIAAA · UNIVERSITY OF SYDNEY · PI Greg Trevor Sutherland · 2012 to 2026
$7.0M
BRAIN TISSUE RESOURCE CENTER FOR ALCOHOL RESEARCHR24AA012725 · NIAAA · UNIVERSITY OF SYDNEY · PI KRIL, JILLIAN JUNE · 2000 to 2011
$2.2M
NIAAA NIH HHS R24 AA012725NIAAA NIH HHS R28 AA012725
6 · The paper itself

Abstract

The pathogenesis of Alzheimer's disease (AD) remains to be elucidated. Oxidative damage and excessive beta-amyloid oligomers are components of disease progression but it is unclear how these factors are temporally related. At post mortem, the superior temporal gyrus (STG) of AD cases contains plaques, but displays few tangles and only moderate neuronal loss. The STG at post mortem may represent a brain region that is in the early stages of AD or alternately a region resistant to AD pathogenesis. We evaluated expression profiles and activity of endogenous anti-oxidants, oxidative damage and caspase activity in the STG of apolipoprotein ε4-matched human AD cases and controls. Total superoxide dismutase (SOD) activity was increased, whereas total glutathione peroxidase (GPX), catalase (CAT) and peroxiredoxin (Prx) activities, were decreased in the AD-STG, suggesting that hydrogen peroxide accumulates in this brain region. Transcripts of the transcription factor NFE2L2 and inducible HMOX1, were also increased in the AD-STG, and this corresponded to increased Nuclear factor erythroid 2-related factor (NRF-2) and total heme-oxygenase (HO) activity. The protein oxidation marker 4-hydroxynonenal (4-HNE), remained unchanged in the AD-STG. Similarly, caspase activity was unaltered, suggesting that subtle redox imbalances in early to moderate stages of AD do not impact STG viability.

Indexed as

Oxidative StressAlzheimer DiseaseAntioxidantsCaspasesFemaleGene Expression ProfilingHumansMaleTemporal LobeAntioxidantsCaspases

Identifiers

PMID30068908
PMCPMC6070512
OpenAlexW2883810413

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.