Journal of Neuroimmunology, Vol. 128 (1-2) (2002) pp. 95-100
T. van Veen a,b, N.F. Kalkers a, J.B.A. Crusius c, L. van Winsen a, F. Barkhof d, P.J.H. Jongen e, A.S. Peña c, C.H. Polman a and B.M.J. Uitdehaag a,b
a Department of Neurology, VU Medical Centre, De Boelelaan 1117, 1007 MB Amsterdam, The Netherlands
b Department of Clinical Epidemiology and Biostatistics, VU Medical Centre, De Boelelaan 1117, 1007 MB Amsterdam, The Netherlands
c Laboratory of Gastrointestinal Immunogenetics, VU Medical Centre, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands
d MS-MRI Centre, VU Medical Centre, De Boelelaan 1117, 1007 MB Amsterdam, The Netherlands
e Stichting Multiple Sclerosis Centrum, 6533 PA Nijmegen, The Netherlands
Several studies have reported a defective Fas function in patients with multiple sclerosis (MS).
We were interested whether this could result from a genetically altered Fas regulation.
We examined the FAS670 polymorphism in 382 patients with MS and 206 controls, and found that the carriership of allele FAS670*G was significantly less frequent in patients than in controls.
We found no association between the carriership of FAS670*G and clinical features.
For a subgroup of patients, longitudinal MRI data were available.
We observed similar brain and lesion volumes in carriers and noncarriers of FAS670*G.
These data suggest that FAS670*G decreases the risk of developing MS, but does not affect the course of disease.
© Copyright 2002, Elsevier Science