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高脂肪饮食通过抑制SIRT1/AMPK介导的自会导致认知障碍
Wenmin Yi1, Fei Chen2, Minghao Yuan2
1The fifth Clinical College of Chongqing Medical University, Chongqing 402160, China; Department of Neurology, Chongqing General Hospital, Chongqing 400013, China; Chongqing Key Laboratory of Neurodegenerative Diseases, Chongqing 400013, China; Chongqing Medical University, Chongqing 400016, China; Chongqing School, University of Chinese Academy of Sciences, Chongqing 400799, China.
高脂肪饮食会通过破坏SIRT1/AMPK通路和自来损害小鼠的记忆和学习,导致高酸化和突触损伤. 这项研究阐明了饮食引起的认知衰退背后的关键机制.
科学领域:
- 神经科学是一个神经科学.
- 代谢研究的研究.
- 老龄化研究研究.
背景情况:
- 高脂肪饮食 (HFD) 越来越多地与认知能力下降有关.
- 机制包括降低突触可塑性和高酸化,但尚未完全理解.
研究的目的:
- 研究Sirtuin1 (SIRT1) /AMP激活蛋白激酶 (AMPK) 途径在HFD诱导的认知障碍中的作用.
- 探索HFD对陶酸化和突触功能的影响.
主要方法:
- 在22周的时间里,小鼠接受了标准或高度食;Neuro-2a细胞接受了棕酸 (PA) 治疗.
- 使用莫里斯水迷宫 (MWM) 评估认知功能.
- 蛋白质水平,陶酸化和自被分析通过西方涂抹和免疫光学.
主要成果:
- HFD诱导的学习和记忆缺陷,突触标记物 (Syn,BDNF) 的降低,以及 fosforylation 的增加.
- HFD降低了SIRT1表达,抑制了AMPK酸化,并影响了自.
- 激活SIRT1在细胞中部分逆转了这些效应.
结论:
- 高酸抑制SIRT1/AMPK通路并破坏自,导致酸过酸化和突触功能障碍.
- 这些分子变化有助于与年龄相关的认知衰退.
- 准SIRT1/AMPK通路可能为饮食引起的认知障碍提供治疗策略.
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