Bax-ablation attenuates experimental autoimmune encephalomyelitis in mice

Nirit Lev, Yael Barhum, Eldad Melamed, Daniel Offen*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Multiple sclerosis (MS) is an inflammatory disease of the central nervous system characterized by demyelination and axonal damage. Although the exact pathophysiology is unknown, apoptosis plays a crucial role. Here, we studied the role of the pro-apoptotic gene Bax in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), the animal model for MS. We demonstrate that the clinical signs were markedly reduced in the EAE Bax-deficient mice as compared to wild type (2.3±0.5 vs. 1.02±0.32, respectively, P<0.05). Bax-deficient mice demonstrated less inflammatory infiltration and axonal damage, although they showed similar T-cell immune potency. In conclusion, ablation of the bax gene attenuates the severity of MOG-induced EAE and emphasizes the importance of apoptosis in the pathogenesis of EAE and MS.

Original languageEnglish
Pages (from-to)139-142
Number of pages4
JournalNeuroscience Letters
Issue number3
StatePublished - 15 Apr 2004


  • Apoptosis
  • Bax-deficient mice
  • Experimental autoimmune encephalomyelitis
  • Multiple sclerosis
  • Myelin oligodendrocyte glycoprotein


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