Nat Neurosci:老药新用!抗肿瘤药或可治疗自闭症

2018-03-17 Tierna 生物探索

目前药物治疗尚无法改变自闭症的病程,也缺乏治疗核心症状的特异性药物,现有药物只能改善患者的一些情绪和行为症状。近日,发表在《Nature Neuroscience》杂志上的一篇文章称,一种抗肿瘤药物或适用于逆转与自闭症谱系障碍(ASD)相关的社会缺陷。

目前药物治疗尚无法改变自闭症的病程,也缺乏治疗核心症状的特异性药物,现有药物只能改善患者的一些情绪和行为症状。近日,发表在《Nature Neuroscience》杂志上的一篇文章称,一种抗肿瘤药物或适用于逆转与自闭症谱系障碍(ASD)相关的社会缺陷。

抗癌药物开发的其中一种策略是通过有效地分离基因,使其能再次被表达,如罗米地辛,它能有效地抑制组蛋白去乙酰酶(HDACs),修饰组蛋白,重新塑造染色质,调节靶向基因的转录。

根据布法罗大学科学家们的说法,受罗米地辛影响的基因,同时作用于癌症和自闭症。仅用极低剂量的罗米地辛对Shank3基因缺陷而患有自闭症的小鼠模型进行短暂的治疗,就可持续抑制它们的社会缺陷障碍。

这种药物的影响在小鼠身上能够持续三周,即从小鼠模型的青少年时期到青少年晚期,相当于人类的几年,这段时间也是社交关展的关键阶段,其结果表明了罗米地辛会对自闭症有一个持久的治疗效果。

1 罗米地辛缓解社会缺陷

在自闭症小鼠模型中,HDAC2异常高,使得细胞核中的染色质非常紧密,阻止了遗传物质进入需要表达的转录机制。

“HDAC抑制剂可以放松高密度的染色质,使转录机制能够进入基因的启动子区域;因此,它们可以被表达出来,一旦HDAC2被上调,它就会减少不应该被抑制的基因,并导致行为上的改变,比如孤独症样的社会缺陷。”纽约州立大学布法罗分校的生理学和生物物理学教授Zhen Yan博士解释说。

罗米地辛的短暂治疗缓解了shank3缺陷小鼠的社会缺陷。“通过在这些小鼠中上调HDAC2转录,然后利用罗米地辛在前额叶皮质中敲除HDAC2,能够挽救它们的社交缺陷。”文章的作者指出。

Yan博士及其同事早期的研究揭示了如何通过影响NMDA(n-甲基-d-天冬氨酸受体)受体的功能来阻断神经通讯继而导致ASD中常见的社会缺陷倾向,这也是调节认知和情绪的关键因素。

研究人员详细描述了Shank3缺陷小鼠中β-连环蛋白(一种调节细胞粘附和转录的Shank3结合蛋白)的核定位增加如何诱导HDAC2上调并导致出现社会缺陷。作者指明,“在下游分子水平上,罗米地辛处理提高了Grin2a和肌动蛋白调控基因的表达和组蛋白乙酰化,并恢复了Shank3缺陷小鼠中的NMDA受体功能和肌动蛋白丝。”

2 罗米地辛的普遍效应

“孤独症涉及到很多基因的缺失,”Yan博士说,“为了挽救这种社交缺陷,必须有一种化合物,使其能够影响到各种参与神经通讯的基因。”

“而自闭症和患癌症风险的基因具有广泛重叠性,其中许多是染色质重塑因子,这一事实也证明了将用于癌症治疗的表观遗传药物作为治疗自闭症的靶向疗法的必要性。”

当Yan博士和她的合著者进行全基因组筛查时,他们发现罗米地辛恢复了200多个被他们用以抑制孤独症动物模型的基因。

3 重要研究结果

“能够调整一组被识别为引发自闭症的关键基因的优势可能解释了这种治疗孤独症的药物的强大功效。”Yan博士说,“本研究的结果强调了与Shank3基因缺陷有关的社会缺陷的表观遗传机制,这可能暗示了对患有Shank3突变的自闭症患者的潜在治疗策略。”

原始出处:
Luye Qin, Kaijie Ma, Zi-Jun Wang, et al. Social deficits in Shank3-deficient mouse models of autism are rescued by histone deacetylase (HDAC) inhibition. Nature Neuroscience. Published online:12 March 2018.

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    2018-06-23 liye789132251
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    2018-03-19 lsndxfj
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    2018-03-19 xiongke014
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    2018-03-18 易水河

    发掘老药也是个好课题啊!

    0

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    2018-03-17 Ramsey

    慢慢的大家发现更多的一药多用

    0

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    2018-03-17 清风拂面

    谢谢分享学习

    0

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