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.