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Neuron:冰桶挑战三周年!研究人员首次发现"渐冻症"的致病突变

2017-08-21 佚名 生物探索

由圣犹达儿童研究医院和梅奥诊所的科学家领导的小组确定了一种基本的生物机制,一种名为TIA1的蛋白突变,会影响蛋白的相变行为,造成控制肌肉的神经元死亡,进而导致ALS。



肌萎缩侧索硬化症(ALS),又称渐冻症,是一种患者的脊髓和大脑逐渐萎缩的病症。2014年夏天,“冰桶挑战”风靡一时,也让更多的人了解和关注ALS,目前尚无有效的治疗方法。恰逢“冰桶挑战”三周年,8月16日发表在Neuron杂志上一项研究或许为开发出有效的治疗ALS的方法提供了可能。

由圣犹达儿童研究医院和梅奥诊所的科学家领导的小组确定了一种基本的生物机制,一种名为TIA1的蛋白突变,会影响蛋白的相变行为,造成控制肌肉的神经元死亡,进而导致ALS。

当研究人员分析受ALS / FTD影响的家庭的基因组时,发现了TIA1突变。Taylor博士表示,这是首次发现ALS的致病突变。与其他遗传疾病不同,这种突变不会在生物调节途径中破坏酶。相反,这种突变会导致与细胞相分离过程有关的TIA1蛋白异常。

相分离是细胞正常发挥功能所依赖的一种机制,细胞内蛋白会通过相分离机制组装成有序的组合体——一种对细胞功能的实现至关重要的无膜细胞器,而TIA1突变会影响蛋白与其他蛋白结合的能力,破坏蛋白相变的平衡,造成细胞器内的TIA1突变蛋白不断增多、聚集,进而杀死控制肌肉的神经元。

研究人员进一步研究发现,ALS患者中TIA1突变经常发生。他们还发现携带这种突变的人也患有这种疾病。Taylor博士表示:“这篇论文提供了第一个确凿的证据,表明导致疾病的突变会改变蛋白质的相变行为。而相变行为的改变也改变了细胞的生物学特性。”

目前ALS的药物,只能试图改善已经受损的神经元的功能,效果甚微。而最新研究结果表明,通过恢复患者体内细胞相分离的平衡,或可避免神经损伤。这为发现ALS/FTD的首个有效治疗方法提供了一条非常有前景的途径。

泰勒及其同事将会继续了解相变的基本过程。同时,相变的基本病理也可能是其他比如说阿尔茨海默氏症等神经退化性疾病的基础,这种研究方法或许也可以应用于阿尔茨海默氏症的研究。

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    2017-11-13 by2021
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    2017-08-27 坚强007

    学习了

    0

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    2017-08-22 xjy02
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    2017-08-22 QQ25ed180f

    进一步学习了-

    0

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    2017-08-22 海棠胜雪

    学习了

    0

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