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周围的粉样β清除介导非酒精性脂肪肝疾病的认知障碍

Xiaobo Peng¹, Xing Zhang², Zihui Xu¹

¹Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, School of Public Health, Tongji Medical College, Huazhong University of Science & Technology, Wuhan 430030, China; Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science & Technology, Wuhan 430030, China.

|March 20, 2024

概括

非酒精性脂肪性肝病 (NAFLD) 损害了肝脏清除β-粉样蛋白 (Aβ) 的能力,导致认知能力下降. 低密度脂蛋白受体相关蛋白1 (LRP-1) 在这个过程中起着关键作用.

科学领域:

肝病学和神经病学肝病学和神经病学
代谢障碍和认知功能
疾病的分子机制.

背景情况:

非酒精性脂肪肝 (NAFLD) 是认知障碍的一个重要危险因素.
大脑粉样β (Aβ) 积累,认知衰退的标志,可能源于外周Aβ清除受损.
肝脏在外周Aβ清除中的作用及其与NAFLD诱导的认知障碍的联系需要阐明.

研究的目的:

在大鼠模型中调查NAFLD严重程度,Aβ积累和认知表现之间的相关性.
评估NAFLD对肝脏Aβ清除的影响以及低密度脂蛋白受体相关蛋白1 (LRP-1) 的作用.
检查NAFLD和LRP-1多态性在人体血Aβ水平上的相互作用.

主要方法:

对NAFLD严重程度,Aβ水平和雌性Sprague-Dawley大鼠的认知功能进行相关分析.
使用培养肝细胞和HepG2细胞进行体外研究,以评估肝脏Aβ清除率和LRP-1功能.
一项人体病例控制研究 (549例NAFLD病例,549例对照) 调查NAFLD,LRP-1 rs1799986多态,以及血Aβ水平.

主要成果:

在老鼠中,NAFLD的严重程度与血和脑Aβ增加以及认知缺陷相关.
NAFLD大鼠显示肝脏LRP-1和Aβ水平降低,与Aβ度和认知表现相反相关.
在体外,棕酸损害了LRP-1表达和Aβ吸收,可以通过PPARα激动剂逆转.
人类研究:NAFLD与血Aβ40 (8.24%) 和Aβ42 (10.51%) 的增加有关.
LRP-1 rs1799986的多态性改变了NAFLD和血Aβ水平之间的关联.

结论:

低密度脂蛋白受体相关蛋白1 (LRP-1) 调解了NAFLD对外围Aβ清除的有害影响.
在NAFLD中LRP-1功能受损有助于Aβ在大脑中的积累,加剧认知障碍.
准LRP-1可能为与NAFLD相关的认知功能障碍提供治疗策略.

关键词:

这就是Aβ积累的过程.认知障碍认知障碍是一种认知障碍.在LRP-1中使用LRP-1.这是NAFLD.周围的Aβ清除值.rs1799986 多形态的多态化

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