Okuda Yoshinobu, Sakoda Saburo
Department of Neurology, D-4, Osaka University Graduate School of Medicine.
Nihon Rinsho. 2003 Aug;61(8):1323-8.
Experimental autoimmune encephalomyelitis(EAE), an inflammatory demyelinating disease of the central nervous system(CNS) provoked by myelin antigens, is widely used as a model for multiple sclerosis. Recent studies have shown that apoptosis may contribute to the death of oligodendrocytes and/or neurons, a pathological event leading to neurological deficits. On the other hand, the apoptotic elimination of inflammatory cells such as T cells and macrophages from the CNS is generally believed to contribute to the spontaneous recovery of EAE. Thus, apoptosis is involved in the disease-regulating as well as the disease-promoting processes of EAE.