http://www.neurology.org/cgi/content/abstract/57/5/853
Neurology 2001;57:853-857
© 2001 American Academy of
Neurology
F. Fazekas, MD;, S. Strasser–Fuchs, MD;, H. Kollegger, MD;, T. Berger, MD;, W. Kristoferitsch, MD;, H. Schmidt, MD;, C. Enzinger, MD;, M. Schiefermeier, PhD;, C. Schwarz, MD;, B. Kornek, MD;, M. Reindl, PhD;, K. Huber, MD;, R. Grass, MD;, G. Wimmer, MD;, K. Vass, MD;, K. H. Pfeiffer, PhD;, H. P. Hartung, MD; and R. Schmidt, MD
From the Department of Neurology (Drs. Fazekas, Strasser-Fuchs, Hartung, Enzinger, and R. Schmidt) and the Institute of Medical Biochemistry (Dr. H. Schmidt), Karl-Franzens University, Graz; Department of Neurology (Drs. Kolleger, Schiefermeier, Schwarz, Kornek, and Vass), University of Vienna; Department of Neurology (Drs. Berger and Reindl) and Institute of Biostatistics (Dr. Pfeiffer), Leopold-Franzens University, Innsbruck; the SMZ-Ost Donauspital (Drs. Kristoferitsch, Grass, and Wimmer), Vienna; and the Ludwig Boltzmann-Institute for Molecular-Genetic Laboratory Diagnostics (Dr. Huber), SMZ-Ost Donauspital, Vienna, Austria.
Address correspondence and reprint requests to Franz Fazekas, MD, Department of Neurology and MRI Center, Karl-Franzens University, Auenbruggerplatz 22, A-8036 Graz, Austria; e-mail: franz.fazekas@kfunigraz.ac.at
Objective:
The apolipoprotein E (APOE) polymorphism
is known to impact on various neurologic disorders and has differential
effects on the immune system and on CNS repair. Previous findings concerning
a possible modulation of the clinical course of MS have been inconsistent,
however.
Methods:
In a cross-sectional study, the authors
investigated 374 patients with clinically definite MS and a disease duration
of at least 3 years and related their clinical and demographic findings
to the allelic polymorphism of the APOE gene. The genotype distribution
of patients with MS was compared with a cohort of 389 asymptomatic, randomly
selected elderly volunteers.
Results:
The authors found no significant
differences in the distribution of genotypes between patients with MS and
controls. However, patients with MS with the e4
allele (n = 85) had a significantly higher progression index of disability
(0.46 ± 0.4 versus 0.33 ± 0.26; p < 0.004) and a worse
ranked MS severity score (5.1 ± 1.9 versus 5.7 ± 1.7; p =
0.05) than their non-e4
counterparts, despite significantly more frequent long-term immunotherapy
in e4 carriers (74%
versus 58%; p < 0.007). The annual relapse rate in e4
carriers (0.87 ± 0.56) was significantly higher than in patients
with MS without an 4 allele (0.71 ± 0.47; p = 0.03).
Conclusions:
These results suggest no effect of
the APOE genotype on susceptibility to MS, but indicate an association
of the APOE e4 allele
with a more severe course of the disease.
Copyright © 2001 by AAN Enterprises,
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