Evidence map›Paper›PMID 19096157›Full record

ReviewJournal of Alzheimer's disease : JAD2008

The effects of NOS2 gene deletion on mice expressing mutated human AbetaPP.

Carol A Colton, Donna M Wilcock, David A Wink, Judianne Davis, William E Van Nostrand, Michael P Vitek

Open access · greenAbstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

51 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Protein Oxidation in Aging and Alzheimer's Disease Brain.Antioxidants (Basel, Switzerland) · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  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 4 institutions in 1 country.

Carol A ColtonDivision of Neurology, Duke University Medical Center, Durham, NC 27710, USA. glia01@aol.com
Donna M Wilcock
David A Wink
Judianne Davis
William E Van Nostrand
Michael P Vitek
Duke Medical Center · USStony Brook University · USDuke University · USNational Institutes of Health · US

Funding

NEUROPATHOLOGY COREP30AG028377 · NIA · DUKE UNIVERSITY · PI WELSH-BOHMER, KATHLEEN ANNE · 2006 to 2011
$9.6M
Redox Mechanism Process of Nos2 and COX2 in Stroma tumor interactionZIABC010898 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WINK, DAVID · 2009 to 2025
$8.6M
Nitric Oxide as a Modifier of Oxidative StressZIASC007281 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI WINK, DAVID · 2009 to 2025
$8.1M
Triple Transgenic Model of Alzheimer's DiseaseR01AG019780 · NIA · DUKE UNIVERSITY · PI VITEK, MICHAEL PETER · 2002 to 2006
$1.8M
Regulation of neuronal NO by apolipoprotein ER01AG019740 · NIA · DUKE UNIVERSITY · PI COLTON, CAROL ANNE · 2002 to 2006
$1.8M
Dysregulation of the neurovascular unit in Alzheimer's Disease.F32AG030942 · NIA · DUKE UNIVERSITY · PI WILCOCK, DONNA M · 2007 to 2009
$154k
NIA NIH HHS AG030942NIA NIH HHS AG19740NIA NIH HHS AG19780NIA NIH HHS F32 AG030942NIA NIH HHS P30 AG028377NIA NIH HHS R01 AG019740NIA NIH HHS R01 AG019780
6 · The paper itself

Abstract

Nitric oxide synthase 2 (NOS2) and its gene product, inducible NOS (iNOS) play an important role in neuroinflammation by generating nitric oxide (NO), a critical signaling and redox factor in the brain. Although NO is associated with tissue damage, it can also promote cell survival. We hypothesize that during long-term exposure to amyloid-beta (Abeta) in Alzheimer's disease (AD), NO levels fall in the brain to a threshold at which the protective effects of NO cannot be sustained, promoting Abeta mediated damage. Two new mouse models of AD have been developed that utilize this concept of NO's action. These mice express human amyloid-beta protein precursor (AbetaPP) mutations that generate Abeta peptides on a mouse NOS2 knockout background. The APP/NOS2(-/-) bigenic mice progress from Abeta production and amyloid deposition to hyperphosphorylated normal mouse tau at AD-associated epitopes, aggregation and redistribution of tau to somatodendritic regions of neurons and significant neuronal loss including loss of interneurons. This AD-like pathology is accompanied by robust behavioral changes. As APP/NOS2(-/-) bigenic mice more fully model the human AD disease pathology, they may serve as a tool to better understand disease progression in AD and the role of NO in altering chronic neurological disease processes.

Indexed as

Gene DeletionAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsChronic DiseaseHumansInflammationMiceMice, TransgenicMutationNitric Oxide Synthase Type IIAmyloid beta-Protein PrecursorNitric Oxide Synthase Type II

Identifiers

PMID19096157
PMCPMC2667339
OpenAlexW147870220

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.