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对阿尔茨海默病病理的抵抗与神经元中的核肥大有关。

Resistance to Alzheimer's pathology is associated with nuclear hypertrophy in neurons.

作者信息

Riudavets Miguel Angel, Iacono Diego, Resnick Susan M, O'Brien Richard, Zonderman Alan B, Martin Lee J, Rudow Gay, Pletnikova Olga, Troncoso Juan C

机构信息

Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

出版信息

Neurobiol Aging. 2007 Oct;28(10):1484-92. doi: 10.1016/j.neurobiolaging.2007.05.005. Epub 2007 Jun 28.

DOI:10.1016/j.neurobiolaging.2007.05.005
PMID:17599696
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2694127/
Abstract

This study focuses on the morphometric changes of neurons in asymptomatic Alzheimer's disease (AD), a state characterized by the presence of AD lesions in subjects without cognitive impairment. In autopsy brains, we used stereological methods to compare the cell body and nuclear volumes of anterior cingulate gyrus (ACG) and CA1 hippocampal neurons in asymptomatic AD subjects (n=9), subjects with AD dementia (AD, n=8), mild cognitive impairment (MCI, n=9), and age-matched controls (controls, n=9). In ACG, we observed a significant decrease in the neuronal volume of MCI and AD compared to controls; by contrast, no atrophy was present in asymptomatic AD. Moreover, we found a significant increase in nuclear volume in asymptomatic AD compared to controls (P<0.001), MCI (P<0.01) and AD (P<0.001) brains. Similar results were found in the CA1 region of the hippocampus. This nuclear hypertrophy may represent an early neuronal reaction to Abeta or Tau, or a compensatory mechanism which forestalls the progression of AD and allows the brain to resist the development of dementia.

摘要

本研究聚焦于无症状阿尔茨海默病(AD)中神经元的形态计量学变化,这种状态的特征是在无认知障碍的受试者中存在AD病变。在尸检大脑中,我们使用体视学方法比较了无症状AD受试者(n = 9)、AD痴呆受试者(AD,n = 8)、轻度认知障碍(MCI,n = 9)以及年龄匹配的对照组(对照组,n = 9)前扣带回(ACG)和海马CA1区神经元的细胞体和细胞核体积。在ACG中,我们观察到与对照组相比,MCI和AD组的神经元体积显著减小;相比之下,无症状AD组未出现萎缩。此外,我们发现与对照组(P<0.001)、MCI组(P<0.01)和AD组(P<0.001)的大脑相比,无症状AD组的细胞核体积显著增加。在海马CA1区也发现了类似结果。这种核肥大可能代表神经元对淀粉样蛋白或tau蛋白的早期反应,或者是一种代偿机制,可延缓AD的进展并使大脑抵抗痴呆的发展。

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本文引用的文献

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