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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Complement upregulation and activation on motor neurons and neuromuscular junction in the SOD1 G93A mouse model of familial amyotrophic lateral sclerosis.
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Complement upregulation and activation on motor neurons and neuromuscular junction in the SOD1 G93A mouse model of familial amyotrophic lateral sclerosis.

机译：在家族性肌萎缩性侧索硬化症的SOD1 G93A小鼠模型中，对运动神经元和神经肌肉接头的补体上调和激活。

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摘要

Complement activation products are elevated in cerebrospinal fluid, spinal cord and motor cortex of patients with amyotrophic lateral sclerosis (ALS) but are untested in models. We determined complement expression and activation in the SOD1 G93A mouse model of familial ALS (fALS). At 126days, C3 mRNA was upregulated in spinal cord and C3 protein accumulated in astrocytes and motor neurons. C3 activation products C3b/iC3b were localized exclusively on motor neurons. At the neuromuscular junction, deposits of C3b/iC3b and C1q were detected at day 47, before the appearance of clinical symptoms, and remained detectable at symptomatic stage (126days). Our findings implicate complement in the denervation of the muscle endplate by day 47 and destruction of the neuromuscular junction and spinal neuron loss by day 126 in the SOD1 G93A mouse model of fALS.
机译：肌萎缩性侧索硬化症（ALS）患者的脑脊液，脊髓和运动皮层中的补体激活产物升高，但未在模型中进行测试。我们确定了家族性ALS（fALS）的SOD1 G93A小鼠模型中的补体表达和激活。在126天时，脊髓中C3 mRNA上调，星形胶质细胞和运动神经元中C3蛋白积聚。 C3激活产物C3b / iC3b仅位于运动神经元上。在神经肌肉接头处，在出现临床症状之前的第47天就检测到C3b / iC3b和C1q的沉积物，并且在有症状的阶段（126天）仍可检测到。我们的发现暗示，在fALS的SOD1 G93A小鼠中，第47天时神经端板的去神经支配和第126天时神经肌肉接头的破坏和脊髓神经元的丧失。

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