|
Sign In to gain access to subscriptions and/or personal tools.
|
Multiple Sclerosis, Vol. 8, No. 2,
98-103 (2002)
DOI: 10.1191/1352458502ms787oa
© 2002 SAGE Publications
APOE genotypes and disease severity in multiple sclerosis
T Masterman
Division of Neurology, NEUROTEC, Karolinska Institutet at Huddinge University Hospital, Stockholm S-141 86, Sweden, thomas.masterman{at}neurotec.ki.se
Z Zhang
Section for Disease Genetics and Bioinformatics, Department of Molecular Sciences, AstraZeneca R&D Södertälje, Stockholm S-141 57, Sweden
D Hellgren
Section for Disease Genetics and Bioinformatics, Department of Molecular Sciences, AstraZeneca R&D Södertälje, Stockholm S-141 57, Sweden
H Salter
Section for Disease Genetics and Bioinformatics, Department of Molecular Sciences, AstraZeneca R&D Södertälje, Stockholm S-141 57, Sweden
M Anvret
Department of Molecular Sciences, AstraZeneca R&D Södertälje, Stockholm S-141 57, Sweden
L Lilius
Division of Geriatric Medicine, NEUROTEC, Karolinska Institutet at Huddinge University Hospital, Stockholm S-141 57, Sweden
L Lannfelt
Division of Geriatric Medicine, NEUROTEC, Karolinska Institutet at Huddinge University Hospital, Stockholm S-141 57, Sweden
J Hillert
Division of Neurology, NEUROTEC, Karolinska Institutet at Huddinge University Hospital, Stockholm S-141 86, Sweden
Apolipoprotein E (apoE) is involved in the transport of lipids necessary for membrane repair and is encoded by a gene on chromosome 19q13, a region positive for linkage in two multiple sclerosis (MS) genome-wide screens. The APOE e4 allele confers susceptibility to both familial and sporadic Alzheimer’s disease (AD). Carriage of e4 is associated with defective dendritic remodeling in AD, and with unfavorable clinical outcome in head trauma and cerebrovascular disease. According to the results of previous studies, APOE e4 does not increase the risk of developing MS, but it may influence disease progression and ultimate disability. From a total cohort of over 900 MS patients, we compared APOE e2-4 genotypes in, roughly, the cohort’s least disabled and most disabled septiles. ‘Benign MS’ (n=124) was defined as an Expanded Disability Status Scale (EDSS) score of 3.0 or less, despite at least 10 years of disease duration, and ‘severe MS’ (n=140) as the attainment of an EDSS score of 6.0 within 8 years of disease onset. We found no significant differences in genotype or phenotype frequencies between the benign-MS and severe-MS septiles; however, the risk conferred by e4 rose progressively upon comparison of carriage rates in more narrowly defined anti-podal quantiles.
Key Words: apolipoprotein E • genotype • multiple sclerosis • phenotype • polymorphism • prognosis
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
B A Parmenter, D R Denney, S G Lynch, L S Middleton, and L M Harlan
Cognitive impairment in patients with multiple sclerosis: association with the APOE gene and promoter polymorphisms
Multiple Sclerosis,
January 1, 2007;
13(1):
25 - 32.
[Abstract]
[PDF]
|
|
|
|
|
|
|
R. M. Burwick, P. P. Ramsay, J. L. Haines, S. L. Hauser, J. R. Oksenberg, M. A. Pericak-Vance, S. Schmidt, A. Compston, S. Sawcer, R. Cittadella, et al.
APOE epsilon variation in multiple sclerosis susceptibility and disease severity: Some answers
Neurology,
May 9, 2006;
66(9):
1373 - 1383.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M J Sedano, P Calmarza, L Perez, and J M Trejo
No association of apolipoprotein E {epsilon}4 genotype with faster progression or less recovery of relapses in a Spanish cohort of multiple sclerosis
Multiple Sclerosis,
February 1, 2006;
12(1):
13 - 18.
[Abstract]
[PDF]
|
|
|
|
|
|
|
M Pinholt, J L Frederiksen, P S Andersen, and M Christiansen
Apo E in multiple sclerosis and optic neuritis: the Apo E-o4 allele is associated with progression of multiple sclerosis
Multiple Sclerosis,
October 1, 2005;
11(5):
511 - 515.
[Abstract]
[PDF]
|
|
|
|
|
|
|
E. M. Frohman, M. Filippi, O. Stuve, S. G. Waxman, J. Corboy, J. T. Phillips, C. Lucchinetti, J. Wilken, N. Karandikar, B. Hemmer, et al.
Characterizing the Mechanisms of Progression in Multiple Sclerosis: Evidence and New Hypotheses for Future Directions
Arch Neurol,
September 1, 2005;
62(9):
1345 - 1356.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. P. Nathan, A. G. Barsukova, F. Shen, M. McAsey, and R. G. Struble
Estrogen Facilitates Neurite Extension via Apolipoprotein E in Cultured Adult Mouse Cortical Neurons
Endocrinology,
July 1, 2004;
145(7):
3065 - 3073.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B Zakrzewska-Pniewska, M Styczynska, A Podlecka, R Samocka, B Peplonska, M Barcikowska, and H Kwiecinski
Association of apolipoprotein E and myeloperoxidase genotypes to clinical course of familial and sporadic multiple sclerosis
Multiple Sclerosis,
June 1, 2004;
10(3):
266 - 271.
[Abstract]
[PDF]
|
|
|
|
|
|
|
J N. Zwemmer, T van Veen, L van Winsen, G J van Kamp, F Barkhof, C H Polman, and B M. Uitdehaag
No major association of A poE genotype with disease characteristics and MRI findings in multiple sclerosis
Multiple Sclerosis,
June 1, 2004;
10(3):
272 - 277.
[Abstract]
[PDF]
|
|
|
|
|
|
|
N. De Stefano, M. L. Bartolozzi, B. Nacmias, V. Zipoli, M. Mortilla, L. Guidi, G. Siracusa, S. Sorbi, A. Federico, and M. P. Amato
Influence of Apolipoprotein E {epsilon}4 Genotype on Brain Tissue Integrity in Relapsing-Remitting Multiple Sclerosis
Arch Neurol,
April 1, 2004;
61(4):
536 - 540.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Raber
Androgens, ApoE, and Alzheimer's Disease
Sci. Aging Knowl. Environ.,
March 17, 2004;
2004(11):
re2 - re2.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M Niino, S Kikuchi, T Fukazawa, I Yabe, and K Tashiro
Polymorphisms of apolipoprotein E and Japanese patients with multiple sclerosis
Multiple Sclerosis,
August 1, 2003;
9(4):
382 - 386.
[Abstract]
[PDF]
|
|
|
|
