Evidence map›Paper›PMID 19288120›Full record

ReviewActa neuropathologica2009

Oxidatively modified proteins in Alzheimer's disease (AD), mild cognitive impairment and animal models of AD: role of Abeta in pathogenesis.

Rukhsana Sultana, Marzia Perluigi, D Allan Butterfield

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Acta neuropathologica, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 2 pooled it
12.0field-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

109 citing papers in PubMed, 2 syntheses or guidelines pooled it, 209 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
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  17. Disruption of Copper Redox Balance and Dysfunction underEnvironment & health (Washington, D.C.) · 2025
    Article
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  20. Review

49 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

3 authors at 2 institutions in 2 countries.

Rukhsana SultanaDepartment of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506-0055, USA.
Marzia Perluigi
D Allan Butterfield
University of Kentucky · USSapienza University of Rome · IT

Funding

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
Oxidative Dysfunction of LRP at the Blood-brain Barrier in Alzheimer's DiseaseR01AG029839 · NIA · SEATTLE INST FOR BIOMEDICAL/CLINICAL RES · PI BANKS, WILLIAM A · 2008 to 2012
$1.7M
NIA NIH HHS AG-029839NIA NIH HHS AG-05119NIA NIH HHS AG-10836NIA NIH HHS P01 AG005119NIA NIH HHS P01 AG010836NIA NIH HHS R01 AG029839
6 · The paper itself

Abstract

Oxidative stress has been implicated in the pathogenesis of a number of diseases including Alzheimer's disease (AD). The oxidative stress hypothesis of AD pathogenesis, in part, is based on beta-amyloid peptide (Abeta)-induced oxidative stress in both in vitro and in vivo studies. Oxidative modification of the protein may induce structural changes in a protein that might lead to its functional impairment. A number of oxidatively modified brain proteins were identified using redox proteomics in AD, mild cognitive impairment (MCI) and Abeta models of AD, which support a role of Abeta in the alteration of a number of biochemical and cellular processes such as energy metabolism, protein degradation, synaptic function, neuritic growth, neurotransmission, cellular defense system, long term potentiation involved in formation of memory, etc. All the redox proteomics-identified brain proteins fit well with the appearance of the three histopathological hallmarks of AD, i.e., synapse loss, amyloid plaque formation and neurofibrillary tangle formation and suggest a direct or indirect association of the identified proteins with the pathological and/or biochemical alterations in AD. Further, Abeta models of AD strongly support the notion that oxidative stress induced by Abeta may be a driving force in AD pathogenesis. Studies conducted on arguably the earliest stage of AD, MCI, may elucidate the mechanism(s) leading to AD pathogenesis by identifying early markers of the disease, and to develop therapeutic strategies to slow or prevent the progression of AD. In this review, we summarized our findings of redox proteomics identified oxidatively modified proteins in AD, MCI and AD models.

Indexed as

Oxidative StressAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCognition DisordersDisease Models, AnimalHumansOxidation-ReductionProteomicsAmyloid beta-Peptides

Identifiers

PMID19288120
PMCPMC2818870
OpenAlexW1970259736

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.