Evidence map›Paper›PMID 15208783›Full record

ArticleAmerican journal of human genetics2004

Genomewide linkage scan for bipolar-disorder susceptibility loci among Ashkenazi Jewish families.

M Daniele Fallin, Virginia K Lasseter, Paula S Wolyniec, John A McGrath, Gerald Nestadt, David Valle, Kung-Yee Liang, Ann E Pulver

Open access · bronzeAbstract read
In one paragraph

Article in American journal of human genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 3 pooled it
5.2field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 3 syntheses or guidelines pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Meta-analysis in psychiatric genetics.Current psychiatry reports · 2005
    Pooled it
  4. Review
  5. De novo variation in bipolar disorder.Molecular psychiatry · 2021
    Article
  6. Review
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  17. Brain white matter development is associated with a human-specific haplotype increasing the synthesis of long chain fatty acids.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
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  19. Review
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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

8 authors at 2 institutions in 1 country.

M Daniele FallinDepartment of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Virginia K Lasseter
Paula S Wolyniec
John A McGrath
Gerald Nestadt
David Valle
Kung-Yee Liang
Ann E Pulver
Johns Hopkins University · USHoward Hughes Medical Institute · US

Funding

X-LINKED EXTENSION OF THE REVISED HASEMAN-ELSTON ALGORITHM FOR LINKAGE ANALYSISP41RR003655 · NCRR · LOUISIANA STATE UNIV HSC NEW ORLEANS · PI ELSTON, ROBERT C. · 1987 to 2011
$11.5M
HETEROGENEITY OF BIPOLAR DISORDERR01MH058153 · NIMH · JOHNS HOPKINS UNIVERSITY · PI PULVER, ANN E · 1999 to 2003
$3.3M
NCRR NIH HHS P41 RR003655NCRR NIH HHS RR03655NIMH NIH HHS R01 MH058153NIMH NIH HHS R01MH58153
6 · The paper itself

Abstract

The relatively short history of linkage studies in bipolar disorders (BPs) has produced inconsistent findings. Implicated regions have been large, with reduced levels of significance and modest effect sizes. Both phenotypic and genetic heterogeneity may have contributed to the failure to define risk loci. BP is part of a spectrum of apparently familial affective disorders, which have been organized by severity. Heterogeneity may arise because of insufficient data to define the spectrum boundaries, and, in general, the less-severe disorders are more difficult to diagnose reliably. To address the inherent complexities in detecting BP susceptibility loci, we have used restricted diagnostic classifications and a genetically more homogeneous (Ashkenazi Jewish) family collection to perform a 9-cM autosomal genomewide linkage scan. Although they are genetically more homogeneous, there are no data to suggest that the rate of illness in the Ashkenazim differs from that in other populations. In a genome scan of 41 Ashkenazi pedigrees with a proband affected with bipolar I disorder (BPI) and at least one other member affected with BPI or bipolar II disorder (BPII), we identified four regions suggestive of linkage on chromosomes 1, 3, 11, and 18. Follow-up genotyping showed that the regions on chromosomes 1, 3, and 18 are also suggestive of linkage in a subset of pedigrees limited to relative pairs affected with BPI. Furthermore, our chromosome 18q22 signal (D18S541 and D18S477) overlaps with previous BP findings. This research is being conducted in parallel with our companion study of schizophrenia, in which, by use of an identical approach, we recently reported significant evidence for a schizophrenia susceptibility locus in the Ashkenazim on chromosome 10q22.

Indexed as

Genetic LinkageGenetic Predisposition to DiseaseBipolar DisorderChromosomes, Human, Pair 18FemaleGenotypeHumansJewsMalePedigreeSequence Analysis, DNA

Identifiers

PMID15208783
PMCPMC1216055
OpenAlexW1986334270

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.