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味觉受体类型1成员3中介于小鼠的饮食诱导的认知障碍
Keon-Hee Lee1, Jae Won Song2, Chong-Su Kim2
1Department of Food and Nutrition, College of Human Ecology, Seoul National University, Seoul 08826, Republic of Korea; Department of Environmental Health Sciences, Graduate School of Public Health, Seoul National University, Seoul 08826, Republic of Korea.
Life sciences
|October 21, 2023
概括
西方饮食通过激活味觉受体类型1成员3 (TAS1R3) 来损害认知能力. 阻止TAS1R3可以防止饮食引起的认知衰退,这表明它是大脑健康的治疗目标.
科学领域:
- 神经科学是一个神经科学.
- 饮食科学 饮食科学
- 分子生物学分子生物学
背景情况:
- 长期的西方饮食 (WD) 消费,高和脂肪和糖,与认知障碍有关.
- 正确的分子机制驱动WD诱导的认知衰退仍然不完全理解.
- 味觉受体类型1成员3 (TAS1R3),对WD组件有反应,在大脑表达,特别是海马.
研究的目的:
- 调查TAS1R3在中介性认知障碍中的作用,这种障碍是由老鼠长期消费WD引起的.
- 在WD引起的认知功能障碍的背景下,阐明受TAS1R3影响的分子通路.
主要方法:
- 野生类型 (WT) 和Tas1r3淘汰 (KO) 的小鼠在18周内被食正常饮食 (ND) 或WD.
- 用新型物体识别和巴恩斯迷宫测试来评估认知功能.
- 用RNA测序和生物信息学分析来探索潜在的分子机制.
主要成果:
- 在WD上的WT小鼠与ND上的WT小鼠相比,表现出显著的认知障碍.
- 塔斯1r3KO小鼠没有表现出认知障碍,即使在长时间的WD养后.
- 脑部疾病诱导的认知障碍与海马体基因表达的改变有关,包括AMP激活蛋白激酶 (AMPK) 信号和Sirtuin 3表达的变化,氧化应激反应减少和KO小鼠的神经发生增加.
结论:
- TAS1R3在调解与WD消费相关的认知缺陷方面发挥着关键作用.
- 针对TAS1R3是一个潜在的治疗策略,可以预防或减轻WD引起的认知障碍.
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