More MS news articles for Oct 2001

Linkage and association analysis of chromosome 19q13 in multiple sclerosis

Margaret A. Pericak-Vance1, Jacqueline B. Rimmler1, Eden R. Martin (1), Jonathan L. Haines (2, 3), Melissa E. Garcia (3), Jorge R. Oksenberg (4), Lisa F. Barcellos (4), Robin Lincoln (4), Donald E. Goodkin (4) and Stephen L. Hauser (4)
(1)  Center for Human Genetics and Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA
(2)  Program in Human Genetics, 519 Light Hall, Vanderbilt University Medical Center, Nashville, TN 37232-0700, USA
(3)  Program in Human Genetics and Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA
(4)  Department of Neurology, University of California, San Francisco, California, USA

The authors are members of the Multiple Sclerosis Genetics Group. Electronic database information: Marshfield genetic linkage maps,


Multiple sclerosis (MS) is an autoimmune neurological disorder with a complex etiology.

Sibling risk, twin, and adoption studies have demonstrated that genes play a vital role in susceptibility to MS.

Numerous association and linkage studies have implicated the major histocompatibility complex (MHC) as one component of the genetic etiology, but additional loci remain to be identified. Genomic screens have suggested over 50 regions that might harbor these genes, but there has been little agreement between studies.

The one region suggested by all four screens resides within chromosome 19q13. Allelic associations with several markers in this region have also been described.

This region has now been examined in detail in an expanded dataset of MS families from the United States.

Genetic linkage and association were tested with multiple markers in this region using both parametric and non-parametric analyses.

Additional support for an MS susceptibility locus was observed, primarily in families with the MS-associated HLA-DR2 allele.

While consistent, this effect appears to be modest with a maximum ls=1.47, probably representing no more than 10% of the overall genetic effect in MS.

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© Springer-Verlag 2001