Evidence map›Paper›PMID 16262206›Full record

ReviewDialogues in clinical neuroscience2005

Genetic bases for endophenotypes in psychiatric disorders.

Wade H Berrettini

Open access · diamondAbstract readReview
In one paragraph

Review in Dialogues in clinical neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  9. Evidence for broader autism phenotype characteristics in parents from multiple-incidence autism families.Autism research : official journal of the International Society for Autism Research · 2012
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  18. Mapping cortical thickness in children with 22q11.2 deletions.Cerebral cortex (New York, N.Y. : 1991) · 2007
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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.

Wade H BerrettiniDepartment of Psychiatry, Center for Neurobiology and Behavior, University of Pennsylvania, 415 Curie Boulevard, Room 111, Philadelphia, PA 19107, USA. wadeb@mail.med.upenn.edu
University of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This article reviews the concept of an endophenotype, with particular reference to heritability as well as diagnostic specificity. An endophenotype need not be heritable, for example, the possible influence of in utero viral infections for schizophrenia. However, heritability is a useful characteristic for a potential endophenotype, as it can be studied in relation to a plausible candidate gene. It should be noted that the traditional methods of demonstrating heritability, eg, twin studies, can be supplemented with DNA sequence studies, suggesting heritability. Endophenotypes need not be specific to a given nosological class of psychiatric disorders, as these classes do not reflect biological categories. Evidence for two useful schizophrenia endophenotypes, the P50 abnormalities and cognitive deficits, is summarized.

Indexed as

Genetic MarkersGenetic Predisposition to DiseasePhenotypeCognition DisordersEvoked Potentials, AuditoryHumansMental DisordersSchizophreniaGenetic Markers

Identifiers

PMID16262206
PMCPMC3181728
OpenAlexW2137966916

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.