十四、总结
根据ALS这一疾病在SOD1基因突变、自由基氧化损伤、神经毒性作用、兴奋性氨基酸毒性作用、神经微丝异常沉积等相关发病机制中，人们通过建立各种动物模型来探究具体致病机制及寻求有效治疗手段，但现有的动物模型也有一定的局限性：SOD1转基因小鼠适合模拟遗传型ALS患者，研究散发性的ALS意义不大；还存在一些基因突变位点没有进行动物造模研究的情况，而且SOD1、TDP-43、FUS等基因过度表达会引起神经毒性，不能充分反映出动物表达突变基因的特点等。
随着发病机制的不断探索发现，目前动物模型还不能很好地概括全部ALS患者类型，对于根据不同原理建立动物模型还需人们不断探索。目前还没有一种ALS动物模型与人类ALS发病完全一致，未来建立与人类ALS极为相似的动物模型至关重要。
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