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C57BL/6.KOR-ApoE小鼠的综合行为学研究

Comprehensive behavioral study of C57BL/6.KOR-ApoE mice.

作者信息

Ueno Hiroshi, Takahashi Yu, Murakami Shinji, Wani Kenta, Miyazaki Tetsuji, Matsumoto Yosuke, Okamoto Motoi, Ishihara Takeshi

机构信息

Department of Medical Technology, Kawasaki University of Medical Welfare, 288, Matsushima, Kurashiki, Okayama, 701-0193, Japan.

Department of Psychiatry, Kawasaki Medical School, Kurashiki, 701-0192, Japan.

出版信息

Transl Neurosci. 2023 Jun 30;14(1):20220284. doi: 10.1515/tnsci-2022-0284. eCollection 2023 Jan 1.

DOI:10.1515/tnsci-2022-0284
PMID:37396111
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10314129/
Abstract

BACKGROUND

Apolipoprotein E (ApoE) is associated with Alzheimer's disease (AD) and cognitive dysfunction in elderly individuals. There have been extensive studies on behavioral abnormalities in ApoE-deficient (Apoe) mice, which have been described as AD mouse models. Spontaneously hyperlipidemic mice were discovered in 1999 as ApoE-deficient mice due to ApoE gene mutations. However, behavioral abnormalities in commercially available Apoe mice remain unclear. Accordingly, we aimed to investigate the behavioral abnormalities of Apoe mice.

RESULTS

Apoe mice showed decreased motor skill learning and increased anxiety-like behavior toward heights. Apoe mice did not show abnormal behavior in the Y-maze test, open-field test, light/dark transition test, and passive avoidance test.

CONCLUSION

Our findings suggest the utility of Apoe mice in investigating the function of ApoE in the central nervous system.

摘要

背景

载脂蛋白E(ApoE)与阿尔茨海默病(AD)及老年人认知功能障碍有关。对已被描述为AD小鼠模型的载脂蛋白E缺陷(Apoe)小鼠的行为异常进行了广泛研究。1999年,由于ApoE基因突变,自发高脂血症小鼠被发现为ApoE缺陷小鼠。然而,市售Apoe小鼠的行为异常仍不清楚。因此,我们旨在研究Apoe小鼠的行为异常。

结果

Apoe小鼠表现出运动技能学习能力下降以及对高度的焦虑样行为增加。Apoe小鼠在Y迷宫试验、旷场试验、明暗转换试验和被动回避试验中未表现出异常行为。

结论

我们的研究结果表明Apoe小鼠在研究ApoE在中枢神经系统中的功能方面具有实用性。

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Apolipoprotein E and Alzheimer disease: pathobiology and targeting strategies.载脂蛋白 E 与阿尔茨海默病:发病机制与靶向治疗策略。
Nat Rev Neurol. 2019 Sep;15(9):501-518. doi: 10.1038/s41582-019-0228-7. Epub 2019 Jul 31.
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