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首页> 外文期刊>Biochemical and Biophysical Research Communications >Endogenous amyloid-beta mediates memory forgetting in the normal brain
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Endogenous amyloid-beta mediates memory forgetting in the normal brain

机译:内源性淀粉样蛋白 - β在普通脑中介导记忆遗忘

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摘要

Amyloid beta (A beta) is known to be one of the strong candidate molecules for initiating Alzheimer's disease and has been extensively studied in the light of disease pathophysiology. However, it is still elusive what roles A beta play in the normal brain. In this study, we report that A beta is required for memory forgetting in the normal brain. We monitored object recognition memory, and in order to quench soluble A beta, we microinjected anti-A beta antibody (4G8) into the ventricles after memory acquisition. Microinjection of anti-A beta antibody prolonged the maintenance of object recognition memory. This effect appeared not to be due to modulation of memory consolidation since antibody injection after memory consolidation still had a similar effect on memory maintenance. Furthermore, the maintenance of object recognition memory was prolonged in Fcgr2b KO mice, which lacks IgG Fc gamma receptor II-b (Fc gamma RIIb), a receptor for soluble A beta oligomers. Taken together, these findings suggest that endogenous A beta is involved in memory forgetting in the normal brain. (C) 2018 Elsevier Inc. All rights reserved.
机译:已知淀粉样蛋白β(β)是用于启动阿尔茨海默病的强烈候选分子之一,并且在疾病病理生理学的光线上被广泛研究。然而,它仍然难以捉摸了β在普通大脑中的角色。在这项研究中,我们报告说,在普通脑中记忆遗忘需要β。我们监测了对象识别存储器,并且为了淬灭ββ,我们在记忆采集后将抗β抗体(4G8)微目影抗β抗体(4G8)进入心室。抗Aβ抗体的显微注射延长了物体识别记忆的维护。这种效果似乎不是由于内存整合后记忆合并的调节,因为内存整合仍然对内存维护具有类似的影响。此外,在FCGR2B KO小鼠中延长对象识别存储器的维持,其缺乏IgGFcγ受体II-B(FcγRIIB),一种用于可溶性β低聚物的受体。在一起,这些研究结果表明内源性β在普通脑中涉及记忆遗忘。 (c)2018年Elsevier Inc.保留所有权利。

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