The pathobiology of Alzheimer's disease.

The pathobiology of Alzheimer's disease.
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DOI:
10.1146/annurev.me.40.020189.000401
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发表时间:
1989
影响因子:
10.5
通讯作者:
G. Glenner
G. Glenner
中科院分区:
医学1区
文献类型:
--
作者:
G. Glenner

文献摘要

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β蛋白是斑块和脑血管的淀粉样纤维以及神经原纤维缠结的成对螺旋细丝的主要成分,它的发现为破解阿尔茨海默病的发病机制提供了一种手段。在老年唐氏综合症患者中,同样的病变也被证明是由β蛋白组成的。基因探针将β蛋白的基因以及家族性阿尔茨海默病的基因定位在21号染色体上,但这些基因并不相连。对695个氨基酸的β蛋白基因前体的翻译后修饰的研究,特别是对异常蛋白降解的研究,可能会为阿尔茨海默病淀粉样变性损害的原因和阻止它们的方法提供见解。
The discovery of beta protein, the major component of the amyloid fibrils of the plaques and cerebral vessels and of the paired helical filaments of the neurofibrillary tangles, has provided a means to decipher the pathogenesis of Alzheimer's disease. The same lesions in aged Down's syndrome individuals have also been shown to be composed of beta protein. Gene probes localize the gene for beta protein, as well as that for familial Alzheimer's disease, to chromosome 21, but these genes are not linked. A study of posttranslational modifications of the 695-amino-acid beta-protein gene precursor, with specific reference to abnormal proteolysis, may provide insights into the cause of the amyloidotic lesions of Alzheimer's disease and the means of arresting them.