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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >A mouse model of subcortical vascular dementia reflecting degeneration of cerebral white matter and microcirculation
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A mouse model of subcortical vascular dementia reflecting degeneration of cerebral white matter and microcirculation

机译：脑白质反射变性的皮下血管性痴呆症的小鼠模型及微循环

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Subcortical vascular dementia(SVaD) is associated with white matter damage, lacunar infarction, and degeneration of cerebral microcirculation. Currently available mouse models can mimic only partial aspects of human SVaD features. Here, we combined bilateral common carotid artery stenosis (BCAS) with a hyperlipidaemia model in order to develop a mouse model of SVaD; 10- to 12-week-old apolipoprotein E (ApoE)-deficient or wild-type C57BL/6J mice were subjected to sham operation or chronic cerebral hypoperfusion with BCAS using micro-coils. Behavioural performance (locomotion, spatial working memory, and recognition memory), histopathological findings (white matter damage, microinfarctions, astrogliosis), and cerebral microcirculation (microvascular density and blood-brain barrier (BBB) integrity) were investigated. ApoE-deficient mice subjected to BCAS showed impaired locomotion, spatial working memory, and recognition memory. They also showed white matter damage, multiple microinfarctions, astrogliosis, reduction in microvascular density, and BBB breakdown. The combination of chronic cerebral hypoperfusion and ApoE deficiency induced cognitive decline and cerebrovascular pathology, including white matter damage, multiple microinfarctions, and degeneration of cerebral microcirculation. Together, these features are all compatible with those of patients with SVaD. Thus, the proposed animal model is plausible for investigating SVaD pathophysiology and for application in preclinical drug studies.
机译：皮质血管痴呆（SVAD）与白质损伤，腔隙性梗死和脑微循环变性有关。目前可用的鼠标模型可以仅模仿人类SVAD功能的部分方面。在这里，我们将双侧常见的颈动脉狭窄（BCA）与高脂血症模型组合，以开发SVAD的小鼠模型;使用微线圈与BCA进行10至12周龄载脂蛋白E（ApoE） - 缺血或野生型C57BL / 6J小鼠的假手术或慢性脑低血量灌注。研究了行为性能（运动，空间工作记忆和识别记忆），组织病理学发现（白质损伤，微量罚，十字间隙症）和脑微循环（微血管密度和血脑屏障（BBB）完整性）。对BCA进行的帕福缺陷小鼠显示出障碍物，空间工作记忆和识别存储器受损。他们还显示出白质损伤，多种微型罚球，十字间隙，微血管密度降低，以及BBB分解。慢性脑低渗和ApoE缺乏诱导的认知下降和脑血管病理学的组合，包括白质损伤，多种微量罚球和脑微循环的退化。这些特征在一起，与SVAD患者兼容。因此，所提出的动物模型是可言可用于研究SVAD病理生理学和在临床前药物研究中的应用。

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