Journal Of Neuroimmunology, cilt.143, sa.1, ss.129-132, 2003 (SCI-Expanded)
A genome screen for linkage disequilibrium in Turkish multiple sclerosis
M. Eraksoya,*,1, A. Hensiekb,1, M. Kurtuncua,b, G. Akman-Demira, M. Kılıncc,
M. Gedizlioglud, B. Petek-Balcıe, O¨ . Anlarf, C. Kutlug, G. Saruhan-Direskenelih,
H.A. I˙drisoglua, E. Setakisi, A. Compstonb, S. Sawcerb
The Turkish Multiple Sclerosis Genetics Study Group (TMSGSG)
a Department of Neurology, Istanbul Faculty of Medicine, University of Istanbul, Capa, Istanbul TR-34390, Turkey
b Neurology Unit, Addenbrooke’s Hospital, University of Cambridge, Cambridge CB2 2QQ, UK
c Department of Neurology, Faculty of Medicine, University of Baskent, Ankara, Turkey
d Department of Neurology, Buca Social Security Hospital, I˙zmir, Turkey
e Department of Neurology, Haseki State Hospital, Istanbul, Turkey
f Department of Neurology, Faculty of Medicine, University of Yu¨zu¨ncu¨ yıl, Van, Turkey
g Department of Neurology, Faculty of Medicine, University of Osmangazi, Eskisehir, Turkey
h Neuroimmunology Laboratory, Department of Physiology, Istanbul Faculty of Medicine, University of Istanbul, Istanbul, Turkey
iMRC Biostatistics Unit, Institute of Public Health, University Forvie Site, Cambridge, UK
Abstract
In order to screen the Turkish population for evidence of association with multiple sclerosis, we typed 6000 microsatellite markers in
separately pooled DNA samples from 197 cases and 199 controls following the Genetic Analysis of Multiple sclerosis in EuropeanS
(GAMES) protocol. Twelve markers showing evidence for association were identified. One of these markers lying directly in a region which
is also implicated in the Turkish linkage screen (chromosome 5p15) and thus shows evidence for both linkage and association in independent
data sets.
D 2003 Elsevier B.V. All rights reserved.
Keywords: Multiple sclerosis; Turkey; Linkage disequilibrium; Genome screen
1. Introduction
Available epidemiological evidence indicates that several
genes determine susceptibility to multiple sclerosis with
each contributing only modest effect individually (Compston,
2000). In this complex situation, tests for association
are significantly more powerful than those based on linkage
and a genome-wide effort to find association by testing all
possible variants systematically would be the ideal experiment
(Collins et al., 1997; Risch and Merikangas, 1996).
Direct screening