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Science:战胜阿尔茨海默氏症不是梦?

2014-04-29 佚名 科学网

2004 年,经验丰富的结构生物学家 Gregory Petsko 和 Dagmar Ringe 曾致力于寻找治愈阿尔茨海默氏症的方法,但结果令人沮丧。 Petsko 说:“我们没能找到治愈疾病的新方法。” 之后,在一场于美国科罗拉多州举办的会议上,他们听取了哥伦比亚大学神经病学家 Scott Small 对其研究的阐述。 Small 对因神经退行性疾病死亡的患者大脑进行了研究。 Pet

2004 年,经验丰富的结构生物学家 Gregory Petsko 和 Dagmar Ringe 曾致力于寻找治愈阿尔茨海默氏症的方法,但结果令人沮丧。 Petsko 说:“我们没能找到治愈疾病的新方法。”

之后,在一场于美国科罗拉多州举办的会议上,他们听取了哥伦比亚大学神经病学家 Scott Small 对其研究的阐述。 Small 对因神经退行性疾病死亡的患者大脑进行了研究。 Petsko 说:“ Small 的研究涉及到一种复杂的分子复合物 retromer ,它在细胞中的作用如同一座回收站,为我们提供了新思路。”

在听取报告的当天, Petsko 、 Ringe 与 Small 共进午餐,并决定开展为期 10 年的合作研究,以研制可以治愈阿尔茨海默氏症的药物,相关研究结果发表在近日的《自然-化学生物学》上。新药物能够通过稳定 retromer 的组成部分,从而降低甚至终止一种名为 β-淀粉样蛋白的蛋白质片段在患者大脑中传播,而后者很可能是导致患者神经死亡的元凶。尽管从最初阶段到现在,该研究都只专注于细胞研究,但其成果仍令其他许多研究阿尔茨海默氏症的专家印象深刻。

海马体是人类大脑处理记忆的关键区域,早在 10 年前 Small 就发现,组成 retromer 的一种关键成分在阿尔茨海默氏症患者海马体中的含量少于它在其他正常区域的含量。 retromer 是一种蛋白质复合体,它包裹着能帮助自身在细胞内部和外膜之间进行循环的细胞表面蛋白,例如 β-淀粉样蛋白的前体细胞。约99%的阿尔茨海默氏症患者大脑内的 β-淀粉样蛋白出现增多,但没有迹象显示是出于遗传原因, Small 的发现则恰好有助于解释这一问题。

随着蛋白片段的溢出,淀粉样前体蛋白( APP )被迫发生分裂, Small 认为这一过程在一处名为核内体的细胞器中发生。他根据其大脑研究提出了一种假设:缺少 retromer 将导致更多 APP 徘徊在核内体周围,使得酶能处理更多的 β-淀粉样蛋白。事实上,阿尔茨海默氏症患者的核内体通常会发生肿大。 Small 说:“ APP 在核内体周围呆得太久了。所以嘭的一声,酶开始分裂。”

然而在 2004 年,科学家尚不清楚 retromer 的缺乏究竟是大脑失调的原因还是结果,而证明其是原因的证据是在过去10年的研究中逐渐得来的。研究者将老鼠体内的一段 retromer 基因移除后发现 β-淀粉样蛋白显著增多,并导致老鼠有记忆缺陷。此外,一些与 retromer 有关的基因发生变异将加大老鼠患上阿尔茨海默氏症的风险。纽约市西奈山医学院神经病学家 Samuel Gandy 说:“一些研究结果仍属于推断,但重要的是没有人能对 Small 的研究模型予以反驳。”

尽管 Small 当时致力于建立阿尔茨海默氏症 retromer 紊乱的档案,但 Petsko 、 Ringe 及研究生Vincent Mecozzi决定设计一种“陪护”化合物来协助稳定 retromer 复杂的结构,从而增加 retromer 在大脑中的总量。这3人都来自马萨诸塞州沃尔瑟姆市布兰迪斯大学。他们利用结构生物学方法,在相互连接的 retromer 蛋白复合物上找到了一处弱点——单个化合物能够在此处与 retromer 紧密地粘贴在一起,从而起到稳定 retromer 和降低细胞退化速度的作用。经过数年研究,他们终于找到了需要的化合物,从某种程度来说这一过程顺利得出乎意料。

针对人工培育的海马神经元的实验发现, Petsko 等人发现的小分子能大大增加 retromer 的数量,增幅达50%甚至更多。此外,它还能降低患有阿尔茨海默氏症的老鼠神经元中 β-淀粉样蛋白的含量。 Gandy 说:“研发一种能提升 retromer 含量的药物是一个绝妙的点子,如果你问我是否曾想到从 retromer 入手治愈阿尔茨海默氏症,我的回答是没有。时间和临床试验将证明这种治疗手段是否可行。”

但是,不加选择地回收细胞中的分子也会带来副作用,因为 APP 中并不只携带 retromer 。 Small 说,治疗的目的在于扭转病态的系统,让 retromer 的活性恢复到正常水平。但他也承认,新药物最终也可能增加健康细胞的“货物流通”,这将造成未知的负面影响。 Small 说:“这些都是我们正在积极应对的重大问题。”

此外,新药物能否成功还依赖于一个推断,即核内体究竟是不是处理大多数 APP 的地方。虽然绝大多数的研究确认了这一推断,但也有一些研究认为 β-淀粉样蛋白被处理的地方位于高尔基复合体,后者的作用在于将蛋白质“打包”后“投送”到其他位置。如果 β-淀粉样蛋白主要在高尔基复合体中被处理,那么提升 retromer 含量的药物将输送更多的 APP ,从而加剧阿尔茨海默氏症的症状,变成“毒药”。

提升 retromer 含量的药物还能作用于帕金森氏症。一段 retromer 基因发生罕见突变后能导致整个家族遗传神经退行性疾病。 Petsko 说:“这让我们所有人都感到吃惊。”他目前供职于纽约市威尔康奈尔医学院,正努力确定帕金森氏症患者神经元中 retromer 的含量。

该研究小组正在提高资金投入以进一步发掘潜在治疗药物,并开始在老鼠身上进行药物试验。 retromer 研究小组深知,研制出一种安全有效的治疗药物非常困难, Petsko 说:“大多数尝试都以失败告终。我可以接受失败,但不能接受没有努力过就失败。”

原始链接:

Ken Garber. Potential Alzheimer's Drug Spurs Protein Recycling. Science, 25 April 2014; DOI:10.1126/science.344.6182.351

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    2014-05-01 jichang
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