Department of Neurology, Department of Laboratory Medicine, Donders Institute for Brain, Cognition and Behaviour, Alzheimer Centre Nijmegen, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands.
J Alzheimers Dis. 2010;22(2):345-55. doi: 10.3233/JAD-2010-100711.
Senile plaques and cerebral amyloid angiopathy in Alzheimer's disease (AD) patients not only consist of the amyloid-β protein (Aβ), but also contain many different Aβ-associated factors, such as heparan sulfate proteoglycans, apolipoproteins, and complement factors. These factors may all influence Aβ deposition, aggregation, and clearance and therefore seem important in the development of human Aβ deposits. To study AD pathology and test new therapeutic agents, many different mouse models have been created. By transgenic expression of the amyloid-β protein precursor, frequently in combination with other transgenes, these animals develop Aβ deposits that morphologically resemble their human counterparts. Whether this resemblance also applies to the presence of Aβ-associated factors is largely unclear. In this review, the co-deposition of factors known to associate with human Aβ deposits is summarized for several different AD mouse models.
阿尔茨海默病（AD）患者的老年斑和脑淀粉样血管病不仅包含淀粉样β蛋白（Aβ），还包含许多不同的 Aβ 相关因子，如硫酸乙酰肝素蛋白聚糖、载脂蛋白和补体因子。这些因子可能都影响 Aβ 的沉积、聚集和清除，因此在人类 Aβ 沉积的发展中似乎很重要。为了研究 AD 的病理学并测试新的治疗剂，已经创建了许多不同的小鼠模型。通过淀粉样前体蛋白的转基因表达，通常与其他转基因结合，这些动物会产生形态上类似于人类的 Aβ 沉积。这种相似性是否也适用于 Aβ 相关因子的存在，在很大程度上尚不清楚。在这篇综述中，总结了几种不同的 AD 小鼠模型中已知与人类 Aβ 沉积相关的因子的共沉积情况。
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