Evidence map›Paper›PMID 17389904›Full record

ArticleMolecular psychiatry2007

Dense SNP association study for bipolar I disorder on chromosome 18p11 suggests two loci with excess paternal transmission.

J G Mulle, M D Fallin, V K Lasseter, J A McGrath, P S Wolyniec, A E Pulver

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Article in Molecular psychiatry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

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0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

7 citing papers in PubMed.

  1. Article
  2. Genome-wide searches for bipolar disorder genes.Current psychiatry reports · 2011
    Article
  3. An investigation of candidate regions for association with bipolar disorder.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2010
    Article
  4. Association between polymorphisms in the metallophosphoesterase (MPPE1) gene and bipolar disorder.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2010
    Article
  5. Article
  6. Review
  7. Family-based SNP association study on 8q24 in bipolar disorder.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2008
    Article
4 · The record

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5 · Who and what money

Authors and funding

6 authors.

J G MulleMcKusick-Nathans Institute of Genetic Medicine, Johns Hopkins School of Medicine, Baltimore, MD 21231, USA.
M D Fallin
V K Lasseter
J A McGrath
P S Wolyniec
A E Pulver

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parent-of-origin effects have been implicated as mediators of genetic susceptibility for a number of complex disease phenotypes, including bipolar disorder. Specifically, evidence for linkage on chromosome 18 is modified when allelic parent-of-origin is accommodated in the analysis. Our goal was to characterize the susceptibility locus for bipolar I disorder on chromosome 18p11 and investigate this parent-of-origin hypothesis in an association context. This was achieved by genotyping single nucleotide polymorphisms (SNPs) at a high density (1 SNP/5 kb) along 13.6 megabases of the linkage region. To increase our ability to detect a susceptibility locus, we restricted the phenotype definition to include only bipolar I probands. We also restricted our study population to Ashkenazi Jewish individuals; this population has characteristics of a genetic isolate and may therefore facilitate detection of variants for complex disease. Three hundred and forty-four pedigrees (363 parent/child trios) where probands were affected with bipolar 1 disorder were genotyped. Transmission disequilibrium test analysis revealed no statistically significant association to SNPs or haplotypes within this region in this sample. However, when parent-of-origin of transmitted SNPs was taken into account, suggestive association was revealed for two separate loci.

Indexed as

Chromosomes, Human, Pair 18Family HealthFather-Child RelationsGenetic Predisposition to DiseaseAllelesBipolar DisorderFemaleGene FrequencyGenotypeHumansJewsLinkage DisequilibriumLongitudinal StudiesMalePolymorphism, Single Nucleotide

Identifiers

PMID17389904

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