Evidence map›Paper›PMID 18648646›Full record

ArticlePloS one2008

iTRAQ analysis of complex proteome alterations in 3xTgAD Alzheimer's mice: understanding the interface between physiology and disease.

Bronwen Martin, Randall Brenneman, Kevin G Becker, Marjan Gucek, Robert N Cole, Stuart Maudsley

Abstract read
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
–field-weighted citation impact
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

61 citing papers in PubMed.

  1. The aggregate proteome ofFrontiers in aging neuroscience · 2025
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Changes in the expression of the B subunit of vacuolar HIranian journal of basic medical sciences · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

1 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

6 authors.

Bronwen MartinLaboratory of Neurosciences, National Institute on Aging Intramural Research Program, Biomedical Research Center, Baltimore, Maryland, United States of America.
Randall Brenneman
Kevin G Becker
Marjan Gucek
Robert N Cole
Stuart Maudsley

Funding

Analysis of complex biological systems by microarray based gene expressionZICAG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI DE, SUPRIYO · 2009 to 2025
$15.5M
Oxidative stresses and complex proteomic responses to themZIAAG000325 · NIA · NATIONAL INSTITUTE ON AGING · PI MAUDSLEY, STUART · 2009 to 2012
$1.4M
Age and pathology-induced alteration of G protein-coupled receptor signalingZIAAG000318 · NIA · NATIONAL INSTITUTE ON AGING · PI MAUDSLEY, STUART · 2009 to 2012
$1.0M
Innate intelligence and prognostication for prevention of neurodegenerationZIAAG000319 · NIA · NATIONAL INSTITUTE ON AGING · PI MAUDSLEY, STUART · 2009 to 2012
$1.0M
Age and pathology-induced alteration of G protein-coupled receptor signalingZ01AG000318 · NIA · NATIONAL INSTITUTE ON AGING · PI MAUDSLEY, STUART · 2007 to 2008
$905k
Analysis of complex biological systems by microarray based gene expressionZ01AG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI BECKER, KEVIN · 2008 to 2008
$886k
Oxidative stresses and complex proteomic responses to themZ01AG000325 · NIA · NATIONAL INSTITUTE ON AGING · PI MAUDSLEY, STUART · 2008 to 2008
$297k
Innate intelligence and prognostication for prevention of neurodegenerationZ01AG000319 · NIA · NATIONAL INSTITUTE ON AGING · PI MAUDSLEY, STUART · 2008 to 2008
$105k
Intramural NIH HHS
6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by progressive cognitive impairment associated with accumulation of amyloid beta-peptide, synaptic degeneration and the death of neurons in the hippocampus, and temporal, parietal and frontal lobes of the cerebral cortex. Analysis of postmortem brain tissue from AD patients can provide information on molecular alterations present at the end of the disease process, but cannot discriminate between changes that are specifically involved in AD versus those that are simply a consequence of neuronal degeneration. Animal models of AD provide the opportunity to elucidate the molecular changes that occur in brain cells as the disease process is initiated and progresses. To this end, we used the 3xTgAD mouse model of AD to gain insight into the complex alterations in proteins that occur in the hippocampus and cortex in AD. The 3xTgAD mice express mutant presenilin-1, amyloid precursor protein and tau, and exhibit AD-like amyloid and tau pathology in the hippocampus and cortex, and associated cognitive impairment. Using the iTRAQ stable-isotope-based quantitative proteomic technique, we performed an in-depth proteomic analysis of hippocampal and cortical tissue from 16 month old 3xTgAD and non-transgenic control mice. We found that the most important groups of significantly altered proteins included those involved in synaptic plasticity, neurite outgrowth and microtubule dynamics. Our findings have elucidated some of the complex proteome changes that occur in a mouse model of AD, which could potentially illuminate novel therapeutic avenues for the treatment of AD and other neurodegenerative disorders.

Indexed as

Gene Expression RegulationAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsHippocampusMaleMiceMice, Inbred C57BLMice, TransgenicMicrotubulesModels, BiologicalNeuronal PlasticityPresenilin-1Proteomicstau ProteinsAmyloid beta-Protein PrecursorPresenilin-1tau Proteins

Identifiers

PMID18648646
PMCPMC2453232

What OpenQuestion holds

Textmetadata
LicenceCC0
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.