Evidence map›Paper›PMID 20049698›Full record

ArticleEMBO molecular medicine2009

More than the sum of its parts: new mouse models for dissecting the genetic complexities of Williams-Beuren syndrome.

Andreas Meyer-Lindenberg

Erratum issuedAbstract readComment
In one paragraph

Article in EMBO molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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

1 author.

Andreas Meyer-LindenbergDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health, University of Heidelberg. a.meyer-lindenberg@zi-mannheim.de

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psychiatric disorders are a common, severe and disabling group of diseases where progress in finding novel molecular targets has been slow. This is partly due to our lack of understanding of the molecular pathophysiology of these conditions as they play out in the brain (Insel & Scolnick, 2006). Since many of these diseases (such as schizophrenia, bipolar disorder or autism) are highly heritable, a genetic approach to dissecting the risk architecture is a promising avenue for molecular medicine; however, variants in single genes frequently present in the population have only small to moderate effects on complex behavioural phenotypes (O'Donovan et al, 2008).

Indexed as

Disease Models, AnimalAnimalsChromosomes, MammalianCognitionHumansMicePhenotypeWilliams Syndrome

Identifiers

PMID20049698
PMCPMC3378111

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.