Evidence map›Paper›PMID 24006891›Full record

ArticleJournal of proteome research2013

Longitudinal study of differential protein expression in an Alzheimer's mouse model lacking inducible nitric oxide synthase.

Michael D Hoos, Brenna M Richardson, Matthew W Foster, Angela Everhart, J Will Thompson, M Arthur Moseley, Carol A Colton

Abstract readComparative Study
In one paragraph

Article in Journal of proteome research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Association of GLOD4 with Alzheimer's Disease in Humans and Mice.Journal of Alzheimer's disease : JAD · 2024
    Article
  3. As a Potential Therapeutic Target, C1q Induces Synapse Loss Via Inflammasome-activating Apoptotic and Mitochondria Impairment Mechanisms in Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    Review
  4. Review
  5. Article
  6. Review
  7. URMC-099 prophylaxis prevents hippocampal vascular vulnerability and synaptic damage in an orthopedic model of delirium superimposed on dementia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  8. Article
  9. Likelihood ratio statistics for gene set enrichment in Alzheimer's disease pathways.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
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  19. Article
  20. mNos2 deletion and human NOS2 replacement in Alzheimer disease models.Journal of neuropathology and experimental neurology · 2014
    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

7 authors at 2 institutions in 1 country.

Michael D HoosDepartment of Medicine/Neurology, ‡Institute for Genome Sciences & Policy, School of Medicine, and §Division of Pulmonary, Allergy and Critical Care Medicine, Duke University Medical Center, Duke University , Durham, North Carolina 27710, United States.
Brenna M Richardson
Matthew W Foster
Angela Everhart
J Will Thompson
M Arthur Moseley
Carol A Colton
Duke University Hospital · USDuke University · US

Funding

The amyloid cascade in a novel mouse model of Alzheimer's diseaseR01AG031124 · NIA · DUKE UNIVERSITY · PI COLTON, CAROL ANNE · 2009 to 2013
$1.5M
A Mouse Model of Inflammation in Alzheimer's DiseaseR01AG031845 · NIA · DUKE UNIVERSITY · PI COLTON, CAROL ANNE · 2009 to 2013
$1.5M
NIA NIH HHS AG031124NIA NIH HHS AG031845NIA NIH HHS R01 AG031124NIA NIH HHS R01 AG031845
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a complex neurodegenerative process that involves altered brain immune, neuronal and metabolic functions. Understanding the underlying mechanisms has relied on mouse models that mimic components of AD pathology. We used gel-free, label-free LC-MS/MS to quantify protein and phosphopeptide levels in brains of APPSwDI/NOS2-/- (CVN-AD) mice. CVN-AD mice show a full spectrum of AD-like pathology, including amyloid deposition, hyperphosphorylated and aggregated tau, and neuronal loss that worsens with age. Tryptic digests, with or without phosphopeptide enrichment on an automated titanium dioxide LC system, were separated by online two-dimensional LC and analyzed on a Waters Synapt G2 HDMS, yielding relative expression for >950 proteins and >1100 phosphopeptides. Among differentially expressed proteins were known markers found in humans with AD, including GFAP and C1Q. Phosphorylation of connexin 43, not previously described in AD, was increased at 42 weeks, consistent with dysregulation of gap junctions and activation of astrocytes. Additional alterations in phosphoproteins suggests dysregulation of mitochondria, synaptic transmission, vesicle trafficking, and innate immune pathways. These data validate the CVN-AD mouse model of AD, identify novel disease and age-related changes in the brain during disease progression, and demonstrate the utility of integrating unbiased and phosphoproteomics for understanding disease processes in AD.

Indexed as

Alzheimer DiseaseAmino Acid SequenceAnimalsBrainChromatography, Ion ExchangeChromatography, Reverse-PhaseHumansLongitudinal StudiesMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutMolecular Sequence DataNitric Oxide Synthase Type IIPhosphopeptidesPhosphorylationcomplement 1q receptorMembrane GlycoproteinsNitric Oxide Synthase Type IINos2 protein, mousePhosphopeptidesProteomeReceptors, Complementtau Proteins

Identifiers

PMID24006891
PMCPMC3875406
OpenAlexW2333417272

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.