Analysis for factors toxic to motor neurons released from astrocytes expressing ALS-linked mutated SOD1.

超氧化物歧化酶-1（SOD1）的突变引起一种致命的麻痹性疾病肌萎缩侧索硬化症（ALS），可能是细胞自主和非细胞自主过程的结合。在这项研究中，我们发现与对照组相比，星形胶质细胞表达突变SOD1（G93A）的初级运动神经元中表达增加的cdna。然后，我们用其中一个在G93A小鼠脊髓运动神经元中表达最多的cdna制作转基因小鼠。它们没有显示运动神经元死亡，因此我们使用的cDNA可能不会导致神经元死亡。

Mutations in superoxide dismutase-1(SOD1) cause a form of the fatal paralytic disorder amyotrophic lateral sclerosis(ALS), presumably by a combination of cell-autonomous and non-cell-autonomous processes. In this study, we identified the cDNAs that expression increased in the primary motor neurons with astrocytes expressing mutated SOD1(G93A) compared to control. Then, we made the transgenic mice with the one of these cDNAs which expressed most in the spinal motor neuron of G93A mice. They did not show the motor neuron death, so this cDNA we used may not cause the neuronal death.