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高脂肪饮食和脑创伤的相互作用会改变脂肪组织巨细胞和与严重的认知功能障碍相关的脑微质

Rebecca J Henry^1,2, James P Barrett¹, Maria Vaida³

¹Department of Anesthesiology and Shock, Trauma and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Baltimore, MD, USA.

bioRxiv : the preprint server for biology

|August 7, 2023

概括

高脂肪饮食肥胖加重创伤性脑损伤 (TBI) 的结果. 结合肥胖和TBI会放大大脑和脂肪组织的炎症,加剧认知缺陷和神经退行.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
代谢障碍代谢障碍代谢障碍

背景情况:

肥胖是一个显著的危险因素,加剧创伤性脑损伤 (TBI) 的结果.
了解肥胖和TBI之间的相互作用对于开发有效的治疗策略至关重要.

研究的目的:

研究高脂肪饮食引起的肥胖 (DIO) 和TBI对中央和外围炎症通路的相互作用影响.
分析大脑和脂肪组织的转录组变化,以阐明由肥胖引起的TBI恶化背后的分子机制.
评估联合DIO和TBI对神经功能和认知缺陷的影响.

主要方法:

成年雄性小鼠在实验性TBI之前和之后被食高脂肪饮食 (HFD) 12周.
用Y-Maze,新型物体识别 (NOR) 和莫里斯水迷宫 (MWM) 测试来评估认知功能.
大脑和内脏脂肪组织 (VAT) 的高通量转录组分析使用纳米链面板进行.
采用了生物信息分析,包括无监督聚类,主要成分分析和IPA途径分析.

主要成果:

结合TBI和HFD导致了附加性认知功能障碍.
转录组分析显示放大了中央 (微质) 和外周 (VAT中的巨细胞) 炎症反应.
肥胖和TBI独立地启动了改变的细胞状态,包括与疾病相关的微质/巨细胞 (DAM) 现型.
相互作用促进了慢性反应性转录基因特征和促炎状态,可能解释了加剧的认知缺陷.

结论:

肥胖和TBI协同促进慢性神经炎症和外周炎症.
针对肥胖诱导的反应性细胞表型,包括脂肪组织巨细胞,可以减轻TBI诱导的神经退行和认知功能障碍.
这些发现强调了代谢健康在TBI恢复中的重要性,并建议针对细胞炎症状态的新疗法.

关键词:

创伤性脑损伤是一种创伤性脑损伤.认知认知认知与疾病相关的微质细胞.微质细胞中的微质细胞神经炎症是一种神经炎症.肥胖症肥胖症肥胖症肥胖症内脏脂肪组织的脂肪组织.

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