Butyrylcholinesterase is associated with β-amyloid plaques in the transgenic APPSWE/PSEN1dE9 mouse model of Alzheimer disease.
Butyrylcholinesterase is associated with β-amyloid plaques in the transgenic APPSWE/PSEN1dE9 mouse model of Alzheimer disease.
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DOI：
10.1097/nen.0b013e31823cc7a6
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发表时间：
2012-01
影响因子：
3.2
通讯作者：
Geula C
中科院分区：
文献类型：
--
作者：
Darvesh S;Cash MK;Reid GA;Martin E;Mitnitski A;Geula C
阿尔茨海默病（AD）脑组织的组织化学分析表明，丁酰胆碱酯酶（BuChE）存在于β淀粉样蛋白（Aβ）斑块中。BuChE在AD病理学中的作用尚不清楚，但形成类似BuChE相关Aβ斑块的动物模型可提供见解。对出现Aβ斑块的APPSWE/PSEN 1dE 9小鼠（ADTg）进行检查，以确定BuChE是否与这些斑块相关，如AD。我们发现，在成熟的ADTg小鼠中，BuChE活性与Aβ斑块相关。Aβ、Thioflavin-S和BuChE阳性斑块主要聚集在嗅结构、大脑皮质、海马结构、杏仁核和小脑。无空斑染色乙酰胆碱酯酶活性。ADTg中斑块染色的分布和丰度与AD中斑块染色的许多方面非常相似。BuChE染色始终显示比Aβ免疫染色检测到的斑块少，但比硫磺素-S观察到的斑块数量多。双标记实验表明，所有BuChE阳性斑块均为Aβ阳性，而只有部分BuChE阳性斑块为硫磺素-S阳性。这些观察结果表明BuChE与Aβ斑块亚群相关，并可能在AD斑块成熟中发挥作用。对该动物模型的进一步研究可以阐明BuChE在AD病理学中的作用。
Histochemical analysis of Alzheimer disease (AD) brain tissues indicates that butyrylcholinesterase (BuChE) is present in β-amyloid (Aβ) plaques. The role of BuChE in AD pathology is unknown but an animal model developing similar BuChE-associated Aβ plaques could provide insights. The APPSWE/PSEN1dE9 mouse (ADTg), which develops Aβ plaques, was examined to determine if BuChE associates with these plaques, as in AD. We found that in mature ADTg mice, BuChE activity associated with Aβ plaques. Aβ-, thioflavin-S- and BuChE-positive plaques mainly accumulated in olfactory structures, cerebral cortex, hippocampal formation, amygdala and cerebellum. No plaques were stained for acetylcholinesterase activity. The distribution and abundance of plaque staining in ADTg closely resembled many aspects of plaque staining in AD. BuChE staining consistently showed fewer plaques than were detected with Aβ immunostaining but a greater number of plaques than were visualized with thioflavin-S. Double-labelling experiments demonstrated that all BuChE-positive plaques were Aβ-positive while only some BuChE-positive plaques were thioflavin-S-positive. These observations suggest that BuChE is associated with a subpopulation of Aβ plaques and may play a role in AD plaque maturation. Further study of this animal model could clarify the role of BuChE in AD pathology.