Evidence map›Paper›PMID 19627988›Full record

ReviewFEBS letters2009

Animal models of human amyloidoses: are transgenic mice worth the time and trouble?

Joel N Buxbaum

Open access · bronzeAbstract readReview
In one paragraph

Review in FEBS letters, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

24 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Experimental methods for studying amyloid cross-interactions.Protein science : a publication of the Protein Society · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Zebrafish model of amyloid light chain cardiotoxicity: regeneration versus degeneration.American journal of physiology. Heart and circulatory physiology · 2019
    Article
  13. Review
  14. Article
  15. Immunoglobulin light chain amyloid aggregation.Chemical communications (Cambridge, England) · 2018
    Review
  16. A library of ATTR amyloidosis patient-specific induced pluripotent stem cells for disease modelling and in vitro testing of novel therapeutics.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2018
    Article
  17. Cellular clearance of circulating transthyretin decreases cell-nonautonomous proteotoxicity inProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  18. Article
  19. Review
  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

1 author at 1 institution in 1 country.

Joel N BuxbaumDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA. jbux@scripps.edu
Scripps Research Institute · US

Funding

Cardiac Amyloidosis in Aging African AmericansR01AG019259 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI BUXBAUM, JOEL N · 2001 to 2012
$5.8M
TRANSTHYRETIN DEPOSITION IN AGING TRANSGENIC MICER01AG015916 · NIA · SCRIPPS RESEARCH INSTITUTE · PI BUXBAUM, JOEL N · 1998 to 2004
$2.5M
Aging and the Tissue Response to Misfolded ProteinsR01AG030027 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI BUXBAUM, JOEL N · 2008 to 2012
$2.1M
NIA NIH HHS AG019259NIA NIH HHS AG030027NIA NIH HHS R01 AG015916NIA NIH HHS R01 AG019259NIA NIH HHS R01 AG030027
6 · The paper itself

Abstract

The amyloidoses are the prototype gain of toxic function protein misfolding diseases. As such, several naturally occurring animal models and their inducible variants provided some of the first insights into these disorders of protein aggregation. With greater analytic knowledge and the increasing flexibility of transgenic and gene knockout technology, new models have been generated allowing the interrogation of phenomena that have not been approachable in more reductionist systems, i.e. behavioral readouts in the neurodegenerative diseases, interactions among organ systems in the transthyretin amyloidoses and taking pre-clinical therapeutic trials beyond cell culture. The current review describes the features of both transgenic and non-transgenic models and discusses issues that appear to be unresolved even when viewed in their organismal context.

Indexed as

Disease Models, AnimalMiceAmyloidosisAnimalsHumansMice, TransgenicProtein Folding

Identifiers

PMID19627988
PMCPMC2749068
OpenAlexW1989119697

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.