Evidence map›Paper›PMID 12509129›Full record

ReviewTransgenic research2002

Transgenesis applied to transmissible spongiform encephalopathies.

Jean-Luc Vilotte, Hubert Laude

Abstract readReview
PubMed Publisher
In one paragraph

Review in Transgenic research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Jean-Luc VilotteLaboratoire de Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78352, Jouy-en-Josas Cedex, France. vilotte@jouy.inra.fr
Hubert Laude

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transmissible spongiform encephalopathies (TSE) are fatal neurodegenerative disorders present in various mammals. TSEs have been studies intensively, even more so following the BSE crisis and the subsequent threat of a human nvCJD epidemic. In the 'protein-only' hypothesis, the infectious agent, called prion, is assumed to be a misfolded host protein. Transgenesis has mainly been applied to study the role of this protein, its structure-function relationship with respect to its pathogenic properties and to assess the genetic origin of the well-recognised species barrier effect. This approach has somewhat supplemented the lack of in vitro models. This review will try to summarise the impressive work that has been done in this field. Although many questions remain unanswered, transgenic experiments have and will still improve our knowledge on this disease and might help us to develop critically needed therapeutic approaches.

Indexed as

AnimalsDisease Models, AnimalGPI-Linked ProteinsHumansMutationPrion DiseasesPrionsSpecies SpecificityTransgenesGPI-Linked ProteinsPrionsPRND protein, human

Identifiers

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.