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More MS news articles for October 2003

Lack of apolipoprotein-E exacerbates experimental allergic encephalomyelitis

http://www.ingenta.com/isis/searching/ExpandTOC/ingenta?issue=infobike://arn/ms/2003/00000009/00000005&index=10

Multiple Sclerosis, 1 October 2003, vol. 9, no. 5, pp. 476-480(5)
Karussis D.[1]; Michaelson D.M.[2]; Grigoriadis N.[1]; Korezyn A.D.[3]; Mizrachi-Koll R.[4]; Chapman S.[2]; Abramsky O.[1]; Chapman J.[3]
[1] Department of Neurology, Laboratory of Neuroimmunology and the Agnes Ginges Center for Neurogenetics, Hadassah Medical Center, Hebrew University, Jerusalem, Israel [2] Department of Neurobiochemistry, Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel [3] Departments of Physiology and Pharmacology, and Neurology, Sieratzki Chair of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel [4] Department of Neurology, Laboratory of Neuroimmunology and the Agnes Ginges Center for Neurogenetics, Hadassah Medical Center, Hebrew University, Jerusalem, Israel

Experimental autoimmune encephalomyelitis (EAE) was found to have a chronic and significantly worse course in apolipoprotein-E (apoE) deficient female mice when compared with matched controls.

Disease measures compared included incidence of EAE (64% versus 31%, P<0.05, c2 test), maximal clinical score (average±SD 2.81±2.5 versus 0.75±1.1, P<0.01, Mann–Whitney test) and mortality (27.3% versus 0%, P=0.02, Mann–Whitney test and c2 test).

ApoE deficient mice had significantly increased lymphocyte proliferation responses to both myelin antigens and mitogens and significantly more infiltrating lesions in the central nervous system (CNS) in histopathology.

Defective neuronal repair mechanisms and enhanced immune reactivity in apoE deficient mice may explain our findings.

Clinical implications for MS are discussed.