Evidence map›Paper›PMID 9588907›Full record

ArticleThe American journal of pathology1998

Reduction in amyloid A amyloid formation in apolipoprotein-E-deficient mice.

M S Kindy, D J Rader

Abstract read
In one paragraph

Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Use of genetic variation as biomarkers for Alzheimer's disease.Annals of the New York Academy of Sciences · 2009
    Review
  7. Article
  8. Article
  9. Review
  10. Inflammation-dependent cerebral deposition of serum amyloid a protein in a mouse model of amyloidosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  11. Review
  12. Article
  13. Article
  14. A protein required for prion generation: [URE3] induction requires the Ras-regulated Mks1 protein.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
  15. Article
  16. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

M S KindyDepartment of Biochemistry, University of Kentucky School of Medicine, and the Veterans Affairs Medical Center, Lexington 40536-0084, USA. mskindy@pop.uky.edu
D J Rader
University of Kentucky · US

Funding

MECHANISMS OF HEAD TRAUMA INDUCED LUNG INJURYP01NS031220 · NINDS · UNIVERSITY OF KENTUCKY · PI YOUNG, ALFRED BYRON · 1994 to 1998
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NIA NIH HHS AG-12860NINDS NIH HHS NS-31220
6 · The paper itself

Abstract

Apolipoproteins have been implicated in the formation of amyloid fibrils. Recent studies have demonstrated that apolipoprotein E (apoE), alone or in combination with apolipoprotein J (apoJ), and other lipoproteins appear to enhance deposition of amyloid fibrils both in systemic and cerebral amyloids, especially Alzheimer's disease (AD). ApoE enhanced the ability of the amyloid beta-protein (1-40) fragment (A beta) to form fibrils in vitro, with apoE4 promoting the greatest fibril formation. ApoE was found associated with both human and mouse amyloid A (AA) deposits. To define the role of apoE in vivo, we utilized mice lacking the apoE gene by gene targeting. We used the AA model in mice to characterize the function of the apoE protein in amyloid fibrillogenesis. ApoE-deficient mice exhibited a decrease in deposition of AA when compared with heterozygous mutant or wild-type animals. In addition, apoE-deficient mice that were injected with an adenovirus that expressed the human apoE3 gene had restored AA deposition and the apoE was associated with the AA fibrils. These results are agreement with the in vitro studies using the beta-peptide and suggest that apoE is not essential for amyloid fibrillogenesis but can promote the development of amyloid deposition.

Indexed as

Acute-Phase ProteinsAdenoviridaeAmyloidosisAnimalsApolipoprotein E3Apolipoproteins EBlotting, SouthernCholesterol, HDLDisease Models, AnimalGlycoproteinsMiceMice, Inbred C57BLMice, KnockoutNucleic AcidsPolymerase Chain ReactionSerum Amyloid A ProteinAcute-Phase Proteinsamyloid enhancing factorApolipoprotein E3Apolipoproteins ECholesterol, HDLGlycoproteinsNucleic AcidsSerum Amyloid A ProteinSilver NitrateTriglycerides

Identifiers

PMID9588907
PMCPMC1858574
OpenAlexW83881960

What OpenQuestion holds

Textmetadata
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.