1 April 2002, vol. 8, no. 2, pp. 98-103(6)
Masterman T; Zhang Z; Hellgren D; Salter H; Anvret M; Lilius L; Lannfelt L; Hillert J
 Division of Neurology, NEUROTEC, Karolinska Institutet at Huddinge University Hospital, Stockholm S-141 86, Sweden
 Section for Disease Genetics and Bioinformatics, Department of Molecular Sciences, AstraZeneca R&D Södertälje, Stockholm S-141 57, Sweden
 Department of Molecular Sciences, AstraZeneca R&D Södertälje, Stockholm S-141 57, Sweden
 Division of Geriatric Medicine, NEUROTEC, Karolinska Institutet at Huddinge University Hospital, Stockholm S-141 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.
© 2002 ingenta