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Rheumatology 2000; 39: 453-456
© 2000 British Society for Rheumatology

Editorials

Peaks and troughs in linkage mapping for the rheumatic diseases

J. S. Lanchbury and N. J. Schork1

Department of Rheumatology, Division of Medicine, 5th Floor Thomas Guy House, Guy's, King's and St Thomas' Hospitals School of Medicine, King's College, Guy's Hospital Campus, London SE1 9RT, UK and
1 Department of Epidemiology and Biostatistics, Case Western Reserve University, Cleveland, Ohio; The Program for Population Genetics and Department of Biostatistics, Harvard University School of Public Health, Boston, Massachusetts; The Jackson Laboratory, Bar Harbor, Maine and The Genset Corporation, La Jolla, California, USA.

The first 150 words of the full text of this article appear below.

Concrete progress in the identification of genes influencing susceptibility and severity in complex rheumatic diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) has been elusive. The last 10 yr has seen the development of the tools and resources for this identification effort and has focused on gene mapping via linkage and association approaches. These ongoing approaches can be crudely reduced to semi-automated electrophoresis apparatus for sizing simple sequence repeats in human DNA, more or less accurate maps of the relative locations of these microsatellite genetic markers across the three billion bases of the human genome, collections of DNA from families with multiple affected cases and statistical methods for linking genetic map positions to disease affection status. RA and SLE are typical examples of diseases of complex aetiology in which the inherited component is only one part of the picture [1]. Risk for disease development is . . . [Full Text of this Article]

Diagnosis and genetic heterogeneity

Problems with family approaches— non-parametric analysis is inefficient

Choice of genetic markers

Current and developing choices


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