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Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1541-1544
Published online before print June 9, 2005, doi: 10.1161/01.ATV.0000173307.25652.89
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1541.)
© 2005 American Heart Association, Inc.

Special Article

Complex Trait Locus Linkage Mapping in Atherosclerosis

Time to Take a Step Back Before Moving Forward?

Rebecca L. Pollex; Robert A. Hegele

From the Robarts Research Institute, London, Ontario, Canada.

Correspondence to Robert A. Hegele, MD, FRCPC, FACP, FAHA, 406-100 Perth Dr, London, Ontario, Canada N6A 5K8. E-mail hegele@robarts.ca


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
Ever since the initial proposal to use polymorphic DNA markers to map genetic diseases,1 linkage analysis (also called "positional cloning") has been used successfully to find the gene defects for hundreds of monogenic Mendelian traits.2 Because monogenic diseases can serve as important models for understanding pathogenesis, especially if they point to novel biochemical and physiological pathways, linkage analysis has revolutionized biomedicine. A prime example of the success of linkage analysis in atherosclerosis was the discovery that ABCA1 was the causative gene for Tangier disease,3 which has created an exciting and thriving new subfield of research. The notable success in localizing the molecular defects in monogenic disorders follows from the simple disease pathogenesis model: a single mutated disease gene is necessary and sufficient to cause the observed trait. A recent search of the Online Mendelian Inheritance in Man (OMIM) human genetic disease database roughly quantifies the extent of this success: by entering the keywords "linkage analysis" AND "autosomal," {approx}900 individual entries were returned. And this likely underestimates the number of monogenic diseases for which the molecular genetic basis was solved by linkage analysis.


*    Applying Linkage Analysis to Complex Traits
 
Buoyed by the successful application of linkage analysis to discover the genetic basis of monogenic diseases, many investigators over the last decade turned their attention to the logical next frontier for human disease gene mapping: susceptibility genes for common complex traits. Clearly, this is an extremely worthy pursuit. Complex traits, such as the end points of common atherosclerosis, affect more people than monogenic diseases and result in an . . . [Full Text of this Article]




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