Apoptosis and MS

[Guest guest]

I have previously indicated that we need to look into an apoptosis

based mechanism for MS and for LDN. These recent studies continue to

support my thinking.

Authors

Lev N. Barhum Y. Melamed E. Offen D.

Institution

Felsenstein Medical Research Center, Beilinson Campus, Tel Aviv

University, Sackler School of Medicine, Petah-Tikva, Israel.

Title

Bax-ablation attenuates experimental autoimmune encephalomyelitis in

mice.

Source

Neuroscience Letters. 359(3):139-42, 2004 Apr 15.

Local Messages

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.