Neurosci Lett. 2004 Apr 15;359(3):139-42
Lev N, Barhum Y, Melamed E, Offen D.
Felsenstein Medical Research Center, Beilinson Campus, Tel Aviv University,
Sackler School of Medicine, Petah-Tikva, Israel.
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.