Evidence map›Paper›PMID 9837839›Full record

ArticleAmerican journal of human genetics1998

Genome screens using linkage disequilibrium tests: optimal marker characteristics and feasibility.

N H Chapman, E M Wijsman

Erratum issuedAbstract read
In one paragraph

Article in American journal of human genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

36 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. An entropy-based statistic for genomewide association studies.American journal of human genetics · 2005
    Article
  20. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

2 authors.

N H ChapmanDepartment of Biostatistics, Department of Medicine, University of Washington, Seattle, USA. nicky@biostat.washington.edu
E M Wijsman

Funding

PREVALENCE /INCIDENCE /RISK FACTORS FOR DEMENTIA ON GUAMP01AG014382 · NIA · UNIVERSITY OF WASHINGTON · PI PERL, DANIEL P · 1997 to 2006
$13.4M
Genomic Analysis of Alzheimer's Disease GenesR37AG011762 · NIA · UNIVERSITY OF WASHINGTON · PI SCHELLENBERG, GERARD DAVID · 2004 to 2013
$2.7M
GENOMIC ANALYSIS OF ALZHEIMERS DISEASE GENESR01AG011762 · NIA · UNIVERSITY OF WASHINGTON · PI SCHELLENBERG, GERARD DAVID · 1994 to 2002
$689k
CLONING OF THE CHROMOSOME 8 WERNERS SYNDROME GENER01AG012019 · NIA · UNIVERSITY OF WASHINGTON · PI SCHELLENBERG, GERARD DAVID · 1994 to 1998
–
NIA NIH HHS AG11762NIA NIH HHS AG 12019NIA NIH HHS AG 14382
6 · The paper itself

Abstract

Linkage disequilibrium (LD) testing has become a popular and effective method of fine-scale disease-gene localization. It has been proposed that LD testing could also be used for genome screening, particularly as dense maps of diallelic markers become available and automation allows inexpensive genotyping of diallelic markers. We compare diallelic markers and multiallelic markers in terms of sample sizes required for detection of LD, by use of a single marker locus in a case-control study, for rare monophyletic diseases with Mendelian inheritance. We extrapolate from our results to discuss the feasibility of single-marker LD screening in more-complex situations. We have used a deterministic population genetic model to calculate the expected power to detect LD as a function of marker density, age of mutation, number of marker alleles, mode of inheritance of a rare disease, and sample size. Our calculations show that multiallelic markers always have more power to detect LD than do diallelic markers (under otherwise equivalent conditions) and that the ratio of the number of diallelic to the number of multiallelic markers needed for equivalent power increases with mutation age and complexity of mode of inheritance. Power equivalent to that achieved by a multiallelic screen can theoretically be achieved by use of a more dense diallelic screen, but mapping panels of the necessary resolution are not currently available and may be difficult to achieve. Genome screening that uses single-marker LD testing may therefore be feasible only for young (<20 generations), rare, monophyletic Mendelian diseases, such as may be found in rapidly growing genetic isolates.

Indexed as

Genetic TestingGenome, HumanAllelesCase-Control StudiesGene FrequencyGenes, DominantGenes, RecessiveGenetic Diseases, InbornGenetic MarkersGenetics, PopulationGenotypeHumansLinkage DisequilibriumModels, GeneticSample SizeSensitivity and SpecificityGenetic Markers

Identifiers

PMID9837839
PMCPMC1377658

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.