Journal article icon

Journal article

A sibling-pair based approach for mapping genetic loci that influence quantitative measures of reading disability.

Abstract:
Family and twin studies consistently demonstrate a significant role for genetic factors in the aetiology of the reading disorder dyslexia. However, dyslexia is complex at both the genetic and phenotypic levels, and currently the nature of the core deficit or deficits remains uncertain. Traditional approaches for mapping disease genes, originally developed for single-gene disorders, have limited success when there is not a simple relationship between genotype and phenotype. Recent advances in high-throughput genotyping technology and quantitative statistical methods have made a new approach to identifying genes involved in complex disorders possible. The method involves assessing the genetic similarity of many sibling pairs along the lengths of all their chromosomes and attempting to correlate this similarity with that of their phenotypic scores. We are adopting this approach in an ongoing genome-wide search for genes involved in dyslexia susceptibility, and have already successfully applied the method by replicating results from previous studies suggesting that a quantitative trait locus at 6p21.3 influences reading disability.
Publication status:
Published

Actions

Access Document

Publisher copy:
10.1054/plef.2000.0187

Authors

More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Human Genetics Wt Centre
Role:
Author


Journal:
Prostaglandins, leukotrienes, and essential fatty acids More from this journal
Volume:
63
Issue:
1-2
Pages:
27-31
Publication date:
2000-01-01
DOI:
EISSN:
1532-2823
ISSN:
0952-3278


Language:
English
Keywords:
Pubs id:
pubs:31744
UUID:
uuid:1ba6c2a5-f504-4200-9c0a-f1916825c36f
Local pid:
pubs:31744
Source identifiers:
31744
Deposit date:
2012-12-19
ARK identifier:

Terms of use


Views and Downloads






If you are the owner of this record, you can report an update to it here: Report update to this record

TO TOP