Evidence map›Paper›PMID 18794890›Full record

SynthesisMolecular psychiatry2010

Population-based linkage analysis of schizophrenia and bipolar case-control cohorts identifies a potential susceptibility locus on 19q13.

C Francks, F Tozzi, A Farmer, J B Vincent, D Rujescu, D St Clair, P Muglia

Open access · bronzeAbstract readMeta-Analysis
PubMed Publisher
In one paragraph

Synthesis in Molecular psychiatry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

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  17. Lentiviral delivery of a vesicular glutamate transporter 1 (VGLUT1)-targeting short hairpin RNA vector into the mouse hippocampus impairs cognition.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014
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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

7 authors at 6 institutions in 5 countries.

C FrancksDivision of Medical Genetics, GlaxoSmithKline, Verona, Italy. clyde.2.francks@gsk.com
F Tozzi
A Farmer
J B Vincent
D Rujescu
D St Clair
P Muglia
GlaxoSmithKline (Italy) · ITCentre for Addiction and Mental Health · CALudwig-Maximilians-Universität München · DEMax Planck Institute for Psycholinguistics · NLPsychiatry Research Trust · GBUniversity of Aberdeen · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Population-based linkage analysis is a new method for analysing genomewide single nucleotide polymorphism (SNP) genotype data in case-control samples, which does not assume a common disease, common variant model. The genome is scanned for extended segments that show increased identity-by-descent sharing within case-case pairs, relative to case-control or control-control pairs. The method is robust to allelic heterogeneity and is suited to mapping genes which contain multiple, rare susceptibility variants of relatively high penetrance. We analysed genomewide SNP datasets for two schizophrenia case-control cohorts, collected in Aberdeen (461 cases, 459 controls) and Munich (429 cases, 428 controls). Population-based linkage testing must be performed within homogeneous samples and it was therefore necessary to analyse the cohorts separately. Each cohort was first subjected to several procedures to improve genetic homogeneity, including identity-by-state outlier detection and multidimensional scaling analysis. When testing only cases who reported a positive family history of major psychiatric disease, consistent with a model of strongly penetrant susceptibility alleles, we saw a distinct peak on chromosome 19q in both cohorts that appeared in meta-analysis (P=0.000016) to surpass the traditional level for genomewide significance for complex trait linkage. The linkage signal was also present in a third case-control sample for familial bipolar disorder, such that meta-analysing all three datasets together yielded a linkage P=0.0000026. A model of rare but highly penetrant disease alleles may be more applicable to some instances of major psychiatric diseases than the common disease common variant model, and we therefore suggest that other genome scan datasets are analysed with this new, complementary method.

Indexed as

Polymorphism, Single NucleotideAdultAgedBipolar DisorderCase-Control StudiesChromosomes, Human, Pair 19Genetic LinkageGenetic Predisposition to DiseaseGenetic TestingGenome-Wide Association StudyHumansMiddle AgedPopulation SurveillanceSchizophrenia

Identifiers

PMID18794890
OpenAlexW2050230619

What OpenQuestion holds

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Registered trials

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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.