Evidence map›Paper›PMID 18628273›Full record

ArticleSchizophrenia bulletin2008

The genetics of symptom-based phenotypes: toward a molecular classification of schizophrenia.

Pamela DeRosse, Todd Lencz, Katherine E Burdick, Samuel G Siris, John M Kane, Anil K Malhotra

Open access · bronzeAbstract read
In one paragraph

Article in Schizophrenia bulletin, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

48 citing papers in PubMed, 93 citations in OpenAlex.

  1. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
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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

6 authors at 3 institutions in 1 country.

Pamela DeRosseCenter for Translational Psychiatry, The Feinstein Institute for Medical Research, Manhasset, NY, USA. pderosse@lij.edu
Todd Lencz
Katherine E Burdick
Samuel G Siris
John M Kane
Anil K Malhotra
Zucker Hillside Hospital · USAlbert Einstein College of Medicine · USYeshiva University · US

Funding

Trials Operation UnitP30MH074543 · NIMH · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI KANE, JOHN M · 2005 to 2009
$8.1M
The Genetics of Psychosis: Towards a Dimensional ApproachR00MH086756 · NIMH · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DEROSSE, PAMELA · 2011 to 2013
$732k
Identifying &Characterizing Prodromal SchizophreniaK01MH065580 · NIMH · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI LENCZ, TODD · 2003 to 2007
$675k
CLINICAL TRIALS IN SCHIZOPHRENIA--MOLECULAR APPROACHESK23MH001760 · NIMH · LONG ISLAND JEWISH MEDICAL CENTER · PI MALHOTRA, ANIL K · 1999 to 2003
$621k
The Genetics of Psychosis: Towards a Dimensional ApproachK99MH086756 · NIMH · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DEROSSE, PAMELA · 2009 to 2010
$156k
NIMH NIH HHS K01 MH065580NIMH NIH HHS K23 MH001760NIMH NIH HHS K99 MH086756NIMH NIH HHS MH001760NIMH NIH HHS MH065580NIMH NIH HHS MH074543NIMH NIH HHS P30 MH074543NIMH NIH HHS R00 MH086756
6 · The paper itself

Abstract

objectiveGenetic linkage studies in schizophrenia (SZ) have primarily focused on the phenotype of disease susceptibility. A limited number of studies, however, have reported suggestive linkage to specific SZ symptom domains including regions on chromosomes 6, 8, and 20. We examined these chromosomal regions for association to positive, negative, and disorganized symptom clusters, using a dense set of single-nucleotide polymorphisms (SNPs).

methodsWe ascertained 178 Caucasian patients with SZ for lifetime severity of clinical symptomatology using a structured diagnostic interview. The cohort was genotyped with the Affymetrix 500K microarray, from which we selected, a priori, 4833 intragenic SNPs located within chromosomal regions previously linked to specific SZ symptom clusters. Parametric tests, corrected for multiple testing, were used to compare the effects of allelic variation within these SNPs to the lifetime severity of the specific symptom domain that had been implicated by prior linkage studies.

resultsWe were able to extend previous reports of linkage between chromosome 6q and both positive and disorganized symptoms. Lifetime severity of positive symptoms was significantly (P = 2.50 x 10(-5)) associated with a SNP within the origin recognition complex subunit 3-like (ORC3L) gene, a gene implicated in synaptic plasticity. Level of disorganized symptoms was significantly (P < 6.00 x 10(-5)) associated 2 SNPs within the brain-specific angiogenesis inhibitor 3 (BAI3) gene, which is highly expressed in brain during development.

conclusionsThese data point toward specific candidate genes located within previously implicated linkage peaks for clinical symptomatology. Identification of functional variants within these regions and a characterization of the effect of these risk genotypes on the treatment of specific clinical symptoms are needed.

Indexed as

PhenotypeSchizophrenic PsychologyAllelesChromosomes, Human, Pair 20Chromosomes, Human, Pair 6Chromosomes, Human, Pair 8Cohort StudiesGenetic LinkageGenetic MarkersGenetic Predisposition to DiseaseGenotypeHumansLod ScoreNerve Tissue ProteinsNeuronal PlasticityOligonucleotide Array Sequence AnalysisADGRB3 protein, humanGenetic MarkersNerve Tissue ProteinsORC3 protein, humanOrigin Recognition Complex

Identifiers

PMID18628273
PMCPMC2632513
OpenAlexW2129950906

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.