Evidence map›Paper›PMID 10924405›Full record

ArticleAmerican journal of human genetics2000

Segregation analysis of phenotypic components of learning disabilities. I. Nonword memory and digit span.

E M Wijsman, D Peterson, A L Leutenegger, J B Thomson, K A Goddard, L Hsu, V W Berninger, W H Raskind

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in American journal of human genetics, 2000. 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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.1field-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

23 citing papers in PubMed, 76 citations in OpenAlex.

  1. Trial
  2. Article
  3. Genome scan for cognitive trait loci of dyslexia: Rapid naming and rapid switching of letters, numbers, and colors.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2014
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Etiologies and molecular mechanisms of communication disorders.Journal of developmental and behavioral pediatrics : JDBP · 2010
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Linkage analyses of chromosomal region 18p11-q12 in dyslexia.Journal of neural transmission (Vienna, Austria : 1996) · 2006
    Article
  18. Genomewide scan for real-word reading subphenotypes of dyslexia: novel chromosome 13 locus and genetic complexity.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2006
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

E M WijsmanDepartments of Medicine and Biostatistics, University of Washington, Seattle, WA, USA. wijsman@u.washington.edu
D Peterson
A L Leutenegger
J B Thomson
K A Goddard
L Hsu
V W Berninger
W H Raskind
Cancer Research Center · USFred Hutch Cancer Center · USCape Town HVTN Immunology Laboratory / Hutchinson Centre Research Institute of South Africa · ZAUniversity of Washington · 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
NCRR NIH HHS 1 P41 RR03655NCRR NIH HHS P41 RR003655PHS HHS P50 33812
6 · The paper itself

Abstract

Dyslexia is a common and complex disorder with evidence for a genetic component. Multiple loci (i.e., quantitative-trait loci [QTLs]) are likely to be involved, but the number is unknown. Diagnosis is complicated by the lack of a standard protocol, and many diagnostic measures have been proposed as understanding of the component processes has evolved. One or more genes may, in turn, influence these measures. To date, little work has been done to evaluate the mode of inheritance of individual component-as opposed to composite-phenotypes, beyond family or twin correlation studies that initially demonstrate evidence for a genetic basis of such components. Here we use two approaches to segregation analysis in 102 nuclear families to estimate genetic models for component phenotypes associated with dyslexia: digit span and a nonword-repetition task. Both measures are related to phonological skills, one of the key component processes in dyslexia. We use oligogenic-trait segregation analysis to estimate the number of QTLs contributing to each phenotype, and we use complex segregation analysis to identify the most parsimonious inheritance models. We provide evidence in support of both a major-gene mode of inheritance for the nonword-repetition task, with approximately 2.4 contributing QTLs, and for a genetic basis of digit span, with approximately 1.9 contributing QTLs. Results obtained by reciprocal adjustment of measures suggest that genes contributing to digit span may contribute to the nonword-repetition score but that there are additional QTLs involved in nonword repetition. Our study adds to existing studies of the genetic basis of composite phenotypes related to dyslexia, by providing evidence for major-gene modes of inheritance of these single-measure component phenotypes.

Indexed as

LanguageAge FactorsChromosome SegregationDyslexiaEnvironmentFingersHumansIntelligence TestsLanguage TestsMemoryModels, GeneticMultifactorial InheritanceNuclear FamilyQuantitative Trait, HeritableSex FactorsStatistics as Topic

Identifiers

PMID10924405
PMCPMC1287523
OpenAlexW2018308896

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.