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阿尔茨海默病与衰老大脑。

Alzheimer's disease and the aging brain.

作者信息

Terry Robert D

机构信息

Department of Neurosciences, University of California, San Diego, CA 92093, USA.

出版信息

J Geriatr Psychiatry Neurol. 2006 Sep;19(3):125-8. doi: 10.1177/0891988706291079.

DOI:10.1177/0891988706291079
PMID:16880353
Abstract

The frequencies of each of the several types of dementia are enumerated, showing that Alzheimer's disease is present in about 80% of cases. Cerebral changes associated with cognitively normal aging include shrinkage of large cortical neurons but not a significant loss of total neuronal number. Nevertheless, the population density of synapses measured by confocal microscopy does decline significantly in normal aging. The classical lesions of Alzheimer's disease are neuritic plaques and neurofibrillary tangles, and their frequency correlates with declining cognitive measures. Although amyloid is prominent in plaques, it is probably not the agent of destruction. That role seems to be held by Abeta oligomers. The strongest structural correlate with cognitive tests is synapse loss, which is probably caused by Abeta oligopeptides in the terminal axons and dendrites.

摘要

列举了几种类型痴呆症各自的发病率,结果显示约80%的病例患有阿尔茨海默病。与认知功能正常的衰老相关的脑部变化包括大脑皮质大神经元萎缩,但神经元总数并无显著减少。然而,通过共聚焦显微镜测量,正常衰老过程中突触的群体密度确实会显著下降。阿尔茨海默病的典型病变是神经炎性斑块和神经原纤维缠结,它们的出现频率与认知功能下降相关。尽管淀粉样蛋白在斑块中很突出,但它可能不是破坏因子。这个角色似乎由β-淀粉样蛋白寡聚体扮演。与认知测试最强的结构关联是突触丧失,这可能是由终末轴突和树突中的β-淀粉样蛋白寡肽引起的。

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