脑淀粉样血管病
高同型半胱氨酸血症
神经科学
动物模型
病理
老年斑
动物研究
血管病
疾病
痴呆
转基因小鼠
医学
转基因
生物
阿尔茨海默病
内科学
风险因素
内分泌学
基因
糖尿病
生物化学
作者
Lieke Jäkel,William E. Van Nostrand,James A. R. Nicoll,David J. Werring,Marcel M. Verbeek
出处
期刊:Clinical Science
[Portland Press]
日期:2017-09-28
卷期号:131 (19): 2469-2488
被引量:55
摘要
Cerebral amyloid angiopathy (CAA), due to vascular amyloid β (Aβ) deposition, is a risk factor for intracerebral haemorrhage and dementia. CAA can occur in sporadic or rare hereditary forms, and is almost invariably associated with Alzheimer’s disease (AD). Experimental (animal) models are of great interest in studying mechanisms and potential treatments for CAA. Naturally occurring animal models of CAA exist, including cats, dogs and non-human primates, which can be used for longitudinal studies. However, due to ethical considerations and low throughput of these models, other animal models are more favourable for research. In the past two decades, a variety of transgenic mouse models expressing the human Aβ precursor protein (APP) has been developed. Many of these mouse models develop CAA in addition to senile plaques, whereas some of these models were generated specifically to study CAA. In addition, other animal models make use of a second stimulus, such as hypoperfusion or hyperhomocysteinemia (HHcy), to accelerate CAA. In this manuscript, we provide a comprehensive review of existing animal models for CAA, which can aid in understanding the pathophysiology of CAA and explore the response to potential therapies.
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