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Progression of amyloid pathology to Alzheimer's disease pathology in an amyloid precursor protein transgenic mouse model by removal of nitric oxide synthase 2.通过去除一氧化氮合酶2，在淀粉样前体蛋白转基因小鼠模型中，淀粉样病理向阿尔茨海默病病理的进展。
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Cerebral microvascular amyloid beta protein deposition induces vascular degeneration and neuroinflammation in transgenic mice expressing human vasculotropic mutant amyloid beta precursor protein.在表达人血管嗜性突变淀粉样前体蛋白的转基因小鼠中，脑微血管淀粉样β蛋白沉积会引发血管变性和神经炎症。
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Early-onset and robust cerebral microvascular accumulation of amyloid beta-protein in transgenic mice expressing low levels of a vasculotropic Dutch/Iowa mutant form of amyloid beta-protein precursor.在表达低水平血管嗜性荷兰型/爱荷华型淀粉样β蛋白前体突变形式的转基因小鼠中，淀粉样β蛋白早期且大量地在脑微血管中积累。
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Microglial tau undergoes phosphorylation-independent modification after ischemia.缺血后小胶质细胞中的tau蛋白发生非磷酸化修饰。
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Pathogenesis of cerebral amyloid angiopathy.脑淀粉样血管病的发病机制。
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Two types of sporadic cerebral amyloid angiopathy.两种散发性脑淀粉样血管病。
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Mechanisms of the antioxidant effects of nitric oxide.一氧化氮抗氧化作用的机制。
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Alzheimer's disease: genes, proteins, and therapy.阿尔茨海默病：基因、蛋白质与治疗
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在缺乏一氧化氮合酶 2 的 Tg-SwDI 小鼠中增强的毛细血管淀粉样血管病相关病变。

Enhanced capillary amyloid angiopathy-associated pathology in Tg-SwDI mice with deleted nitric oxide synthase 2.

机构信息

Department of Neurosurgery, HSC T-12/086, Stony Brook University, Stony Brook, NY 11794-8122, USA.

出版信息

Stroke. 2010 Oct;41(10 Suppl):S135-8. doi: 10.1161/STROKEAHA.110.595272.

DOI:10.1161/STROKEAHA.110.595272
PMID:20876489
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2997647/
Abstract

BACKGROUND AND PURPOSE

Cerebral amyloid angiopathy Type 1 is characterized by amyloid β protein deposition along cerebral capillaries and is accompanied by perivascular neuroinflammation and accumulation of phospho-tau protein. Tg-SwDI mice recapitulate capillary amyloid deposition and associated neuroinflammation but lack accumulation of perivascular phospho-tau protein.

METHODS

Tg-SwDI mice were bred onto a nitric oxide synthase 2 gene knockout background and aged for 1 year. Brains were harvested and analyzed using immunohistochemical and quantitative stereological methods to determine the extent of capillary amyloid deposition, perivascular activated microglia, and cell-specific accumulation of phospho-tau protein. Similar methods were also used to compare Tg-SwDI/NOS2(-/-) and human cerebral amyloid angiopathy Type 1 brain tissues.

RESULTS

The absence of nitric oxide synthase 2 gene had no effect on the regional pattern or frequency of capillary cerebral amyloid angiopathy or the numbers of perivascular activated microglia in Tg-SwDI mice. On the other hand, Tg-SwDI/NOS2(-/-) mice accumulated phospho-tau protein in perivascular neurons and activated microglia. Tg-SwDI/NOS2(-/-) mice exhibited a very similar distribution of capillary amyloid, activated microglia, and perivascular phospho-tau protein as seen in human cerebral amyloid angiopathy Type 1.

CONCLUSIONS

These findings indicate that Tg-SwDI/NOS2(-/-) mice more fully recapitulate the pathological changes observed with capillary amyloid in human cerebral amyloid angiopathy Type 1.

摘要

背景与目的

脑淀粉样血管病 1 型的特征是淀粉样 β 蛋白沿脑毛细血管沉积，并伴有血管周围神经炎症和磷酸化 tau 蛋白的积累。Tg-SwDI 小鼠再现了毛细血管淀粉样沉积和相关的神经炎症，但缺乏血管周围磷酸化 tau 蛋白的积累。

方法

将 Tg-SwDI 小鼠繁殖到一氧化氮合酶 2 基因敲除背景上，并使其老化 1 年。采集大脑并使用免疫组织化学和定量立体学方法进行分析，以确定毛细血管淀粉样沉积、血管周围活化的小胶质细胞以及磷酸化 tau 蛋白的细胞特异性积累的程度。类似的方法也用于比较 Tg-SwDI/NOS2(-/-)和人类脑淀粉样血管病 1 型脑组织。

结果

一氧化氮合酶 2 基因的缺失对 Tg-SwDI 小鼠毛细血管脑淀粉样血管病的区域模式或频率或血管周围活化的小胶质细胞数量没有影响。另一方面，Tg-SwDI/NOS2(-/-)小鼠在血管周围神经元和活化的小胶质细胞中积累了磷酸化 tau 蛋白。Tg-SwDI/NOS2(-/-)小鼠表现出与人类脑淀粉样血管病 1 型中所见非常相似的毛细血管淀粉样、活化的小胶质细胞和血管周围磷酸化 tau 蛋白的分布。

结论

这些发现表明，Tg-SwDI/NOS2(-/-)小鼠更充分地再现了人类脑淀粉样血管病 1 型中观察到的与毛细血管淀粉样相关的病理变化。