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Good And Bad Cell Death

机译:好与坏细胞死亡

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摘要

A major driver of neurodegeneration in Alzheimer's disease is thought to be plaques of amyloid-β peptides. These 40-42-amino-acid fragments form when the transmem-brane amyloid-β precursor protein (APP) is degraded by the enzymes β- and y-secretase. In addition to amyloid-β peptides, degradation of APP results in the formation of other peripheral fragments. Perhaps unsurprisingly, given the compelling link between the deposition of amyloid-β peptides and the development of Alzheimer's disease, these additional fragments have been outshone and have received scant attention. But on page 981 of this issue, Nikolaev and colleagues report that one oft-neglected fragment - the soluble amino-terminal portion of APP (N-APP) - has a crucial role in fine-sculpting of the nervous system during development, and possibly in disease-associated neurodegeneration as well.
机译:人们认为,阿尔茨海默氏病神经退行性病变的主要驱动因素是淀粉样β肽斑块。当跨膜淀粉样β-前体蛋白(APP)被β-和γ-分泌酶降解时,就会形成这些40-42个氨基酸的片段。除β淀粉样蛋白肽外,APP的降解还导致其他外周片段的形成。考虑到淀粉样蛋白-β肽的沉积与阿尔茨海默氏病的发展之间存在着令人信服的联系,也许不足为奇,这些额外的片段已经过时了,受到了很少的关注。但是在此问题的第981页上,尼古拉耶夫及其同事报告说,一个经常被忽略的片段-APP的可溶性氨基末端部分(N-APP)-在发育过程中对神经系统的精细雕刻中起着至关重要的作用,甚至可能在疾病相关的神经变性中也是如此。

著录项

  • 来源
    《Nature》 |2009年第7232期|970-971|共2页
  • 作者

    Donald W. Nicholson;

  • 作者单位
  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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