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PNAS:揭示阿尔茨海默氏症罪魁祸首

2013-08-21 ebiotrade bio360

发表在8月19日《美国科学院院刊》(PNAS)杂志上一项研究表明,铜(Copper)似乎是引起阿尔茨海默氏症(Alzheimer disease,AD)发病,并促进疾病进程的一个主要的环境因子。【原文下载】 研究的主要作者、罗彻斯特大学医学中心(URMC)神经外科研究教授、转化神经医学中心成员 Rashid Deane 博士说:“很显然,随着时间的推移,铜的累积效应损害了将β淀粉样蛋白清

发表在8月19日《美国科学院院刊》(PNAS)杂志上一项研究表明,铜(Copper)似乎是引起阿尔茨海默氏症(Alzheimer disease,AD)发病,并促进疾病进程的一个主要的环境因子。【原文下载

研究的主要作者、罗彻斯特大学医学中心(URMC)神经外科研究教授、转化神经医学中心成员 Rashid Deane 博士说:“很显然,随着时间的推移,铜的累积效应损害了将β淀粉样蛋白清除出大脑的系统。这种损伤是导致蛋白质在大脑累积及形成阿尔茨海默氏症标志性的斑块的一个关键因素。”



铜在食物供应中普遍存在。它被发现存在于铜管输送的饮用水、营养补剂和如红肉、贝壳类动物、坚果和许多的水果及蔬菜等某些食物中。这一矿物质在神经传导、骨生长、结缔组织形成和激素分泌中起着重要及有益的作用。

然而,新研究表明铜也在大脑中累积,造成血脑屏障出现故障,导致细胞活动副产物β淀粉样蛋白毒性累积。利用小鼠和人类脑细胞,Deane和同事们进行了一系列的实验,确定了铜加速阿尔茨海默氏症病状的分子机制。

在正常情况下,一种称作为LRP1(lipoprotein receptor-related protein 1)负责将β淀粉样蛋白清除出大脑。这些蛋白质排列在为大脑供血的毛细血管上,与大脑组织中的β-淀粉样蛋白结合,并护送它们进入血管,将它们清除出大脑。

研究人员在三个月的时间内给予正常小鼠包括有含微量铜的饮用水,其是环境保护局确定的铜水质标准的十分之一。

Deane说:“这些铜的水平非常的低,相当于人们正常饮食消耗的水平,”Deane说。

研究人员发现,铜进入到了血液系统中,并在大脑供血血管中,尤其是在毛细血管的细胞“墙壁”上累积。这些细胞是大脑防御系统的关键组成部分,帮助调控了分子进出脑组织。在此情况下,毛细血管阻止了铜进入大脑。而随着时间推移累积在这些细胞中的铜会产生毒性作用。

研究人员观察发现,铜通过氧化过程破坏了LRP1的功能,转而抑制了清除大脑中的β-淀粉样蛋白。他们在小鼠和人类脑细胞中均观察到了这一现象。

研究人员随后检测了铜接触对于阿尔茨海默氏症小鼠模型的影响。在这些小鼠中,形成血脑屏障的细胞发生故障,变得“易漏”,使得诸如铜等元素能够无阻碍进入到脑组织中。他们观察到,铜激发神经元的活性,促进了β淀粉样蛋白生成。铜还在某种程度上与β淀粉样蛋白相互作用,导致蛋白质结合成更大的复合物,生成了大脑废物处理系统无法清除的蛋白质阻塞。

这一连环出击的组合拳,抑制了β-淀粉样蛋白清除,刺激了其生成,从而提供了强有力的证据表明铜是阿尔茨海默氏症的一个关键作用因子。此外,研究人员还发现,铜引起了脑组织炎症,进一步促进了血脑屏障破坏,和阿尔茨海默氏症毒素累积。

然而研究人员说,由于铜是人类许多其他功能所必需的,这些结果必须要谨慎地进行解析。

Deane说:“铜是一种必不可少的金属,可以明确的是这些效应是由于长期铜接触所致。关键是在太少和太多铜消耗之间维持适当的平衡。现在我们还不能确定适当的水平,但饮食最终可能在调控这一过程中起重要的作用。”

原始出处:

Itender Singh, Abhay P. Sagare, Mireia Coma, David Perlmutter, Robert Gelein,Robert D. Bell, Richard J. Deane, Elaine Zhong, Margaret Parisi, Joseph Ciszewski,R. Tristan Kasper, and Rashid Deane. Low levels of copper disrupt brain amyloid-β homeostasis by altering its production and clearance. PNAS August 19, 2013; doi:10.1073/pnas.1302212110 【原文下载

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    2014-06-21 drwjr
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