rss
J Neurol Neurosurg Psychiatry 2000;69:25-28 doi:10.1136/jnnp.69.1.25
  • Paper

Apolipoprotein E genotype related differences in brain lesions of multiple sclerosis

  1. Franz Fazekasa,b,
  2. Siegrid Strasser-Fuchsa,
  3. Helena Schmidtc,
  4. Christian Enzingera,
  5. Stefan Ropelea,b,
  6. Anita Lechnera,
  7. Erich Flooha,
  8. Reinhold Schmidta,b,
  9. Hans-Peter Hartunga
  1. aDepartment of Neurology, Karl-Franzens University, Auenbruggerplatz 22, A-8036 Graz, Austria, bMRI Institute, Karl-Franzens University, Auenbruggerplatz 9, A-8036 Graz, Austria, cInstitute of Medical Biochemistry, Harrachgasse 21, A-8010 Graz, Austria
  1. Dr Franz Fazekasfranz.fazekas{at}kfunigraz.ac.at
  • Received 6 December 1999
  • Revised 23 February 2000
  • Accepted 6 March 2000

Abstract

OBJECTIVES Clinical reports have speculated on a more severe course of multiple sclerosis in patients with the apolipoprotein E (apoE) ε4 allele. As this could be reflected by differences in the severity of tissue damage MRI was used to obtain further support for a disease modifying effect of the apoE genotype.

METHODS Brain MR scans of 83 patients (mean age 35.5 (SD 9.5 years) who participated in a cross sectional study on the distribution of genotype patterns in multiple sclerosis. The total lesion load on proton density weighted (T2-LL) and T1 weighted scans (T1-LL) obtained with conventional spin echo sequences at 1.5 T was measured. A “black hole” ratio ((T1-LL/T2-LL)×100) was also calculated. This indicates the proportion of multiple sclerosis lesions with more severe tissue damage and may reflect disease aggressiveness or quality of repair.

RESULTS Patients with the apoE-ε3/ε4 genotype (n=19) showed a non-significantly greater T2-LL (16.0 (SD 14.0) cm3) than patients with the ε2/ε3 (n=11; 13.3 (9.5) cm3) or the ε3/ε3 genotype (n=49; 9.4 (SD 9.2) cm3). Both the T1-LL (2.6 (SD 3.3)v 1.6 (SD 2.4) and 1.2 (SD 3.0) cm3; p=0.04) and the black hole ratio (14.3 SD 11.9)v 7.4 (SD 9.3) and 8.4 (SD 13.3)%; p=0.02), however, were significantly higher in ε3/ε4 patients. Similar differences were seen when comparing patients with at least one ε4 allele with the remainder of the group.

CONCLUSIONS These data support speculations on a modulation of multiple sclerosis severity by the apoE genotype which can be attributed to more extensive tissue destruction or less efficient repair in carriers of the ε4 allele.

Footnotes

    This Article

    1. Abstract
    2. Full text
    3. PDF

    Responses

    1. Submit a response
    2. No responses published

    Register for free content

    The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

    Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.

    BMJ Careers - Latest neurology and neurosurgery jobs