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• W2063313555 abstract "Currently, no curative treatment is available for spinal muscular atrophy (SMA). Since the degeneration of spinal motor neurons in SMA is mediated by apoptosis, over-expression of an anti-apoptotic factor, Bcl-x(L), may benefit SMA. Here, we crossed a mouse model of SMA with Bcl-x(L) transgenic mice to create SMA/Bcl-x(L) mice. The Bcl-x(L) expression in the spinal neurons of SMA/Bcl-x(L) mice was nearly double that in SMA mice. SMA/Bcl-x(L) mice showed preserved motor function, normalized electrophysiological tests, diminished muscle atrophy, and less motor neuron degeneration. In addition, the life span of SMA/Bcl-x(L) mice was 1.5 times longer than that of SMA mice. Therefore, over-expression of Bcl-x(L) has a potential for amelioration of SMA, and Bcl-x(L) may be another attractive therapeutic target other than survival motor neuron (SMN) protein for use in future drug screening for SMA." @default.
• W2063313555 created "2016-06-24" @default.
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• W2063313555 date "2008-09-01" @default.
• W2063313555 modified "2023-10-18" @default.
• W2063313555 title "Restoring Bcl-xL levels benefits a mouse model of spinal muscular atrophy" @default.
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• W2063313555 doi "https://doi.org/10.1016/j.nbd.2008.05.014" @default.
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