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Lack of apolipoprotein-E exacerbates experimental allergic encephalomyelitis

Department of Neurology, Laboratory of Neuroimmunology and the Agnes Ginges Center for Neurogenetics, Hadassah Medical Center, Hebrew University, Jerusalem, Israel, karus{at}cc.huji.ac.il

D M Michaelson

Department of Neurobiochemistry, Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel

N Grigoriadis

Department of Neurology, Laboratory of Neuroimmunology and the Agnes Ginges Center for Neurogenetics, Hadassah Medical Center, Hebrew University, Jerusalem, Israel

A D Korezyn

Departments of Physiology and Pharmacology, and Neurology, Sieratzki Chair of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

R Mizrachi-Koll

Department of Neurology, Laboratory of Neuroimmunology and the Agnes Ginges Center for Neurogenetics, Hadassah Medical Center, Hebrew University, Jerusalem, Israel

S Chapman

Department of Neurobiochemistry, Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel

O Abramsky

Department of Neurology, Laboratory of Neuroimmunology and the Agnes Ginges Center for Neurogenetics, Hadassah Medical Center, Hebrew University, Jerusalem, Israel

J Chapman

Departments of Physiology and Pharmacology, and Neurology, Sieratzki Chair of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, 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, x² 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 x² test). A poE 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 histopatho logy. Defective neuronal repair mechanisms and enhanced immune reactivity in apoE deficient mice may explain our findings. C linical implications for MS are discussed.

Key Words: A lzheimer’s disease • apoE • experimental autoimmune encephalomyelitis (EA E) • multiple sclerosis

Multiple Sclerosis, Vol. 9, No. 5, 476-480 (2003)
DOI: 10.1191/1352458503ms950oa


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