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• W2063663247 abstract "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." @default.
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• W2063663247 date "2004-04-01" @default.
• W2063663247 modified "2023-09-25" @default.
• W2063663247 title "Bax-ablation attenuates experimental autoimmune encephalomyelitis in mice" @default.
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• W2063663247 doi "https://doi.org/10.1016/j.neulet.2004.01.076" @default.
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