可以通过激活BDNF/TrkB通路来改善认知障碍.
Yu Liu1, Ye Liu2, Liping Shi3
1Department of Epidemiology and Health Statistics, School of Public Health, Ningxia Medical University, Yinchuan 750004, China; Department of Medical Administration, Baotou Central Hospital, Baotou, Inner Mongolia 014040, China.
概括
补充剂改善了阿尔茨海默氏症患者的记忆和学习.
科学领域:
- 神经科学是一个神经科学.
- 营养生物化学 营养生物化学
背景情况:
- 阿尔茨海默病 (AD) 是一种进展性神经退行性疾病,影响认知,特别是在老年人中.
- 是一种对生理过程至关重要的微量营养素;其缺乏与疾病和加速衰老有关.
- 阿尔茨海默病的认知障碍可能受到等营养因素的影响.
研究的目的:
- 研究在阿尔茨海默病小鼠模型 (3×Tg-AD小鼠) 中改善认知缺陷的治疗潜力.
- 阐明作用背后的分子机制,特别是它与来自大脑的神经营养因子 (BDNF) /热胺受体激酶B (TrkB) 途径的关系.
主要方法:
- 利用3×Tg-AD小鼠模型进行食干预.
- 通过行为实验评估学习和记忆.
- 使用生物化学试验,RT-qPCR和西式涂抹量化,谷氨过氧化酶 (GSH-Px),粉胺-β (Aβ),酸化 (P-tau),BDNF,TrkB和CREB水平;通过传输电子显微镜检查神经元亡.
主要成果:
- 补充剂显著改善了3×Tg-AD小鼠的空间学习和记忆.
- 在被补充的小鼠的大脑组织中观察到和GSH-Px水平的升高,以及神经元完整性的增强.
- 显著增加了BDNF,TrkB和化CREB (p-CREB) 的表达,表明BDNF/TrkB通路的激活.
结论:
- 在阿尔茨海默病的小鼠模型中,饮食有效地改善了认知障碍.
- 的有益作用是通过激活BDNF/TrkB信号通路来实现的.
- 显示出作为一种潜在的治疗药物来管理阿尔茨海默病的认知衰退的承诺.
关键词:
在APP/PS1/tau3×Tg-AD小鼠中.阿尔茨海默氏症是阿尔茨海默氏症的一种疾病.这就是为什么BDNF是BDNF.克里布 (Creb) 是一个非常重要的数字.是一种.这就是为什么TrkBB.更多相关视频
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