新功能、新界面、新体验,扫描即可下载生物谷APP!
首页 » Nature报道 » Nature:阿尔兹海默氏症可传播的证据

Nature:阿尔兹海默氏症可传播的证据

来源:生物谷 2015-09-11 11:54

2015年9月11日 讯 /生物谷BIOON/ --近日,来自伦敦大学的科学家通过研究表示,注射提取自尸体大脑中的激素或可在接种者机体中留下潜在的阿尔兹海默氏症的“种子”,相关研究发表于国际杂志Nature上。文章中研究者表示,组装形成阿尔兹海默氏症斑块的蛋白片段或许会通过疾病组织的转移而传递到其他健康个体中,但这并不表明阿尔兹海默氏症具有传染性。

研究者表示,文章中我们对8名个体的大脑进行研究,这些个体在幼年时接受过激素注射来治疗侏儒症,而这些激素提取自数千名尸体的垂体中;研究者发现,有7名个体大脑中都含有阿尔兹海默氏症相关的β淀粉样蛋白片段的沉着物,其中4名个体大脑中沉着物的浓度较高;更让研究者惊讶的是,这些病人年龄均在36至51岁之间,然而β淀粉样蛋白沉着物正常情况下仅会在老年个体大脑中存在。

因此最可能的解释就是这些患者儿时注射的生长激素制剂,而且这些生长激素制剂或许受到了克雅氏病朊病毒的污染;此前研究表明,当大脑组织中的β淀粉样蛋白被转移到小鼠或者猴子机体中时就会感染宿主动物大脑,因此或许存在多种机制来将这些蛋白转运至大脑中,但研究者并不清楚具体的机制,但有一点很明显,就是这些疾病“种子”会通过肌内注射扩散到患者大脑中。

本文研究指出,8名患者并未出现完全的阿尔兹海默氏症特征,而且其机体中也缺失Tau蛋白引发的杂乱无章的蛋白质缠结现象;因此研究者并不可能知道是否这些个体会继续发病;为此研究者将会继续深入研究,希望找到可以指示人类风险的证据。(生物谷Bioon.com)

本文系生物谷原创编译整理,欢迎转载!转载请注明来源并附原文链接。更多资讯请下载生物谷APP.

 

Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

Zane Jaunmuktane, Simon Mead, Matthew Ellis, Jonathan D. F. Wadsworth, Andrew J. Nicoll, Joanna Kenny, Francesca Launchbury, Jacqueline Linehan, Angela Richard-Loendt, A. Sarah Walker, Peter Rudge, John Collinge & Sebastian Brandner

 

More than two hundred individuals developed Creutzfeldt–Jakob disease (CJD) worldwide as a result of treatment, typically in childhood, with human cadaveric pituitary-derived growth hormone contaminated with prions1, 2. Although such treatment ceased in 1985, iatrogenic CJD (iCJD) continues to emerge because of the prolonged incubation periods seen in human prion infections. Unexpectedly, in an autopsy study of eight individuals with iCJD, aged 36–51 years, in four we found moderate to severe grey matter and vascular amyloid-β (Aβ) pathology. The Aβ deposition in the grey matter was typical of that seen in Alzheimer’s disease and Aβ in the blood vessel walls was characteristic of cerebral amyloid angiopathy3 and did not co-localize with prion protein deposition. None of these patients had pathogenic mutations, APOE ε4 or other high-risk alleles4 associated with early-onset Alzheimer’s disease. Examination of a series of 116 patients with other prion diseases from a prospective observational cohort study5 showed minimal or no Aβ pathology in cases of similar age range, or a decade older, without APOE ε4 risk alleles. We also analysed pituitary glands from individuals with Aβ pathology and found marked Aβ deposition in multiple cases. Experimental seeding of Aβ pathology has been previously demonstrated in primates and transgenic mice by central nervous system or peripheral inoculation with Alzheimer’s disease brain homogenate6, 7, 8, 9, 10, 11. The marked deposition of parenchymal and vascular Aβ in these relatively young patients with iCJD, in contrast with other prion disease patients and population controls, is consistent with iatrogenic transmission of Aβ pathology in addition to CJD and suggests that healthy exposed individuals may also be at risk of iatrogenic Alzheimer’s disease and cerebral amyloid angiopathy. These findings should also prompt investigation of whether other known iatrogenic routes of prion transmission may also be relevant to Aβ and other proteopathic seeds associated with neurodegenerative and other human diseases.

相关会议:2015衰老与疾病研讨会

官方网站:http://www.bioon.com/z/2015AD/

温馨提示:87%用户都在生物谷APP上阅读,扫描立刻下载! 天天精彩!


相关标签

最新会议 培训班 期刊库