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肌萎缩侧索硬化与其他神经变性病重叠的研究进展 被引量:6

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摘要 肌萎缩侧索硬化(ALS)是一种致死性的慢性进行性的神经变性病,病因和发病机制尚未明确,研究表明,其机制可能涉及DNA/RNA和蛋白质稳态破坏、tau蛋白过度磷酸化、炎性反应、铁代谢和钙稳态障碍等.虽然90% ~95%的ALS无家族遗传史,但ALS的不同基因型可影响疾病的治疗、进展及预后,所以目前基因遗传学仍是研究热点.迄今为止,ALS发病相关基因的发病率从高到低依次为C9orf72、SOD1、TARDBP、FUS、ANG、ATXN2、UBQLN2和VCP等基因,其病理学包涵体的主要蛋白有TDP-43、SOD1、FUS和tau等[1].研究发现,ALS与额颞叶痴呆(FTD)、阿尔茨海默病(AD)、帕金森病和包涵体肌病(IBM)等神经变性病在基因、病理学、发病机制、临床表现上有部分重叠.我们通过上述方面对ALS与其他神经变性病重叠的研究进展进行综述.
出处 《中华神经科杂志》 CAS CSCD 北大核心 2015年第5期428-430,共3页 Chinese Journal of Neurology
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共引文献11

同被引文献57

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