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JAD：阿尔茨海默氏症研究获进展

2013-12-19 孙爱民 中国科学报

阿尔茨海默氏症
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阿尔茨海默氏症的并发原因一直是困扰基因组学与遗传学界的科学难题，中国科学院北京基因组研究所研究员雷红星全面分析了国外脑转录组的数据，发现在阿尔茨海默氏症患者的脑部转录组中，第19号染色体区域（chr19p）是最显著扰动的染色体区域，并提出了基因组和转录组两方面的证据，来表明该区域在阿尔茨海默氏症致病机理中起到特殊作用。相关研究成果发表在8月份的《阿尔茨海默氏症》杂志上。【原文下载】 阿尔茨海默氏

阿尔茨海默氏症的并发原因一直是困扰基因组学与遗传学界的科学难题，中国科学院北京基因组研究所研究员雷红星全面分析了国外脑转录组的数据，发现在阿尔茨海默氏症患者的脑部转录组中，第19号染色体区域（chr19p）是最显著扰动的染色体区域，并提出了基因组和转录组两方面的证据，来表明该区域在阿尔茨海默氏症致病机理中起到特殊作用。相关研究成果发表在8月份的《阿尔茨海默氏症》杂志上。【原文下载】

阿尔茨海默氏症，又称老年痴呆症，是一种进行性发展的致死性神经退行性疾病。目前，在全基因组关联研究的背景下，散发性阿尔茨海默氏症的遗传学机理还不是十分清楚。尽管遗传学研究已经确定了包括第19号染色体区域在内的几个与阿尔茨海默氏症显著相关的基因位点，但这些基因位点在阿尔茨海默氏症的致病机理中所起到的功能作用仍待进一步研究。

雷红星及其研究团队基于阿尔茨海默氏症脑部转录组数据分析，找出了那些在散发性阿尔茨海默氏症中具有较大扰动的基因，这些基因被认为在致病机理中有着重要的调控作用。研究人员进一步考察了这些基因在不同染色体区域上的分布情况后，发现chr19p是最显著扰动的染色体区域，而且它包含着chr19p13.2条带区。chr19p13.2在之前的遗传学研究中，被认为是迟发型阿尔茨海默氏症的主要遗传易感区域。

“基因组和转录组两方面的证据都表明了chr19p在阿尔茨海默氏症致病机理中起到的特殊作用，今后研究者们可以更加密切地关注chr19p上的一些变化，这对于未来疾病治疗与药物开发都将有指导意义。”雷红星表示。

原文出处

Wang J, Feng X, Bai Z, Jin LW, Duan Y, Lei H.Chromosome 19p in Alzheimer's disease: when genome meets transcriptome.J Alzheimers Dis. 2014 Jan 1【原文下载】

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    2014-01-03 ms1948154235210413

    #阿尔茨#

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    2014-10-02 axin009

    #研究获进展#

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    2014-04-19 12498da4m32(暂无昵称)

    #阿尔茨海#

    0

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    2014-03-27 zhs3882

    #阿尔茨海默氏#

    0

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    2013-12-21 yhj-time

    #阿尔茨海默#

    0

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日本研究人员一项最新研究成果显示，向患有阿尔茨海默氏症的实验鼠血管中注射一种基因物质，成功使得负责分解β淀粉样蛋白的基因在脑内发挥作用，实验鼠的病症得到明显改善。这使得将来有可能以接种疫苗的形式来预防这种常见疾病。 一种名为脑啡肽酶的分解酶发挥着防止β淀粉样蛋白蓄积的功能，β淀粉样蛋白的蓄积被认为是导致阿尔茨海默氏症的原因。但随着年龄增长，一些人负责生成脑啡肽酶的基因功能出现衰退，从而导致发病。

J Neuroinflammation：阻断过度活化受体恢复阿尔茨海默氏症小鼠记忆功能

近日，一项新的研究表明，老年小鼠阿尔茨海默氏症的病理记忆可以逆转得到恢复治疗。蒙特利尔神经学研究所、麦吉尔大学和蒙特利尔大学的研究人员的研究发现，阻断阿尔茨海默氏病（AD）小鼠大脑中的一个特定的受体的活性，能恢复记忆和脑功能。 研究结果发表在Journal of Neuroinflammation杂志上，新研究揭示了AD的基本机制，并标明该受体可作为一个潜在的新疗法靶标。 神经学家Edith

Nature：阿尔茨海默氏症病因新解读

由美国麻省大学医学院、波恩大学和德国先进欧洲学习与研究中心的研究人员组成的一个国际研究小组，在新研究中证实一个众所周知的免疫炎症过程在阿尔茨海默氏症的病理学中发挥了重要的作用。这一过程导致生成了成熟的促炎性细胞因子白细胞介素1β（IL-1B），与机体抵御感染相关，因此被确立为类风湿性关节炎的一个临床靶点。这一发表在《自然》（Nature）杂志上的研究发现指出了破坏IL-1B生成的药物，例如类风湿性

Nat Commun ：一种新型多肽C99能遏制阿尔茨海默氏症发病

日本同志社大学的一个研究小组宣布，他们开发出一种新物质，能遏制导致阿尔茨海默氏症（早老性痴呆）的β淀粉样蛋白的生成。这一成果将有助于开发出副作用很小的预防和治疗阿尔茨海默氏症的方法。【原文下载】 同志社大学副教授舟本聪率领的研究小组发现，一种酶与一种称为“C99”的蛋白质结合之后形成β淀粉样蛋白。如果遏制这种酶发挥作用，就有可能对阿尔茨海默氏症进行治疗。但是，由于这种

AAIC 2013:灵北及大冢新药Lu AE58054能显著改善AD认知

灵北制药（Lundbeck）和大冢制药（Otsuka）7月17日在波士顿举行的2013年度阿尔茨海默氏症协会国际会议（AAIC 2013）上公布了实验性药物Lu AE58054的首批临床数据。 该II期临床研究是一项多中心、随机、双盲、平行组、安慰剂对照试验，在欧洲、加拿大、澳大利亚等国278例中度阿尔茨海默氏症（Alzheimer's disease，AD）患者中开展，探索了Lu AE58

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