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神经原纤维缠结和斑块在老年三转基因阿尔茨海默病小鼠中并不伴有白质病理学改变。

Neurofibrillary tangles and plaques are not accompanied by white matter pathology in aged triple transgenic-Alzheimer disease mice.

机构信息

Department of Physics, University of Winnipeg, 515 Portage Avenue, Winnipeg, Manitoba, R3B 2E9, Canada.

出版信息

Magn Reson Imaging. 2013 Nov;31(9):1515-21. doi: 10.1016/j.mri.2013.06.013. Epub 2013 Aug 29.

DOI:10.1016/j.mri.2013.06.013
PMID:23993791
Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the most common cause of dementia in aging populations. Although senile plaques and neurofibrillary tangles are well-established hallmarks of AD, changes in cerebral white matter correlate with cognitive decline and may increase the risk of the development of dementia. We used the triple transgenic (3xTg)-AD mouse model of AD, previously used to show that white matter changes precede plaque formation, to test the hypothesis that MRI detectable changes occur in the corpus callosum, external capsule and the fornix. T2-weighted and diffusion tensor magnetic resonance imaging and histological stains were employed to assess white matter in older (11-17months) 3xTg-AD mice and controls. We found no statistically significant changes in white matter between 3xTg-AD mice and controls, despite well-developed neurofibrillary tangles and beta amyloid immunoreactive plaques. Myelin staining was normal in affected mice. These data suggest that the 3xTg-AD mouse model does not develop MRI detectable white matter changes at the ages we examined.

摘要

阿尔茨海默病(AD)是一种进行性神经退行性疾病,是老年人群中痴呆症最常见的病因。虽然老年斑和神经纤维缠结是 AD 的明确标志,但大脑白质的变化与认知能力下降相关,并且可能增加痴呆症的发展风险。我们使用之前用于显示白质变化先于斑块形成的 AD 的三转基因(3xTg)-AD 小鼠模型,来检验 MRI 可检测到的胼胝体、外囊和穹窿变化是否发生的假说。T2 加权和弥散张量磁共振成像和组织学染色用于评估老年(11-17 个月)3xTg-AD 小鼠和对照组的白质。尽管存在发达的神经纤维缠结和β淀粉样免疫反应性斑块,但我们在 3xTg-AD 小鼠和对照组之间没有发现白质有统计学意义上的变化。在受影响的小鼠中髓鞘染色正常。这些数据表明,在我们检查的年龄,3xTg-AD 小鼠模型没有发展出 MRI 可检测到的白质变化。

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