Lack of apolipoprotein-E exacerbates experimental allergic encephalomyelitis

Dimitrios Karussis*, D. M. Michaelson, N. Grigoriadis, A. D. Korezyn, R. Mizrachi-Koll, S. Chapman, O. Abramsky, J. Chapman

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


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, χ2 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 χ2 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.

Original languageEnglish
Pages (from-to)476-480
Number of pages5
JournalMultiple Sclerosis Journal
Issue number5
StatePublished - Oct 2003


  • Alzheimer's disease
  • ApoE
  • Experimental autoimmune encephalomyelitis (EAE)
  • Multiple schlerosis


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