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空气污染和阿尔茨海默病表型会耗尽大脑中酯化促消退脂质介质储备。

Air pollution and Alzheimer disease phenotype deplete esterified proresolving lipid mediator reserves in the brain.

作者信息

Taha Ameer Y, Shen Qing, Otoki Yurika, Liang Nuanyi, Patten Kelley T, Valenzuela Anthony E, Wallis Christopher D, Rowland Douglas J, Chaudhari Abhijit J, Bein Keith J, Wexler Anthony S, Jin Lee-Way, Dugger Brittany N, Harvey Danielle J, Lein Pamela J

机构信息

Department of Food Science and Technology, College of Agriculture and Environmental Sciences.

Center for Neuroscience, and.

出版信息

JCI Insight. 2025 May 13;10(15). doi: 10.1172/jci.insight.175917. eCollection 2025 Aug 8.

DOI:10.1172/jci.insight.175917
PMID:40359012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12348674/
Abstract

BACKGROUNDTraffic-related air pollution (TRAP) is a risk factor for Alzheimer disease (AD), where unresolved brain inflammation has been linked to deficits in the levels of free lipid mediators that enable the resolution of inflammation. It is unknown whether these deficits are due to reductions in esterified lipid pools, the main source of free bioactive proresolving lipids in the brain, and whether they are related AD pathophysiology.METHODSThis unknown was tested by measuring brain esterified lipid mediators and pathogenic markers of AD in TgF344-AD and WT male and female rats exposed to filtered air or TRAP for 14 months; it was also tested in human postmortem prefrontal cortex of individuals with or without AD.RESULTSSignificant reductions in proresolving lipid mediators esterified to neutral lipids and/or phospholipids were seen in AD and TRAP-exposed female rats, where levels were associated with inflammation, synaptic loss, and impaired glucose metabolism. Lower esterified proresolving lipid mediator concentrations were associated with older age in prefrontal cortex of humans with AD compared with controls.CONCLUSIONImpaired resolution in AD is due to depletion of esterified proresolving lipid pools that supply the brain with free bioactive mediators involved in inflammation resolution. TRAP exposure alters the same esterified resolution pathways, reflecting convergent mechanisms underlying AD.

摘要

背景

交通相关空气污染（TRAP）是阿尔茨海默病（AD）的一个风险因素，其中未解决的脑部炎症与能够解决炎症的游离脂质介质水平降低有关。目前尚不清楚这些降低是否归因于酯化脂质池的减少，酯化脂质池是大脑中游离生物活性促解决脂质的主要来源，以及它们是否与AD病理生理学相关。

方法

通过测量暴露于过滤空气或TRAP 14个月的TgF344-AD和野生型（WT）雄性和雌性大鼠的脑酯化脂质介质和AD致病标志物来检验这一未知问题；还在有或没有AD的个体的人类死后前额叶皮质中进行了测试。

结果

在AD和暴露于TRAP的雌性大鼠中，酯化到中性脂质和/或磷脂的促解决脂质介质显著减少，其水平与炎症、突触丧失和葡萄糖代谢受损相关。与对照组相比，AD患者前额叶皮质中较低的酯化促解决脂质介质浓度与年龄较大有关。

结论

AD中解决能力受损是由于酯化促解决脂质池的消耗，这些脂质池为大脑提供参与炎症解决的游离生物活性介质。TRAP暴露改变了相同的酯化解决途径，反映了AD潜在的共同机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd37/12348674/263807c67e08/jciinsight-10-175917-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd37/12348674/aea704907454/jciinsight-10-175917-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd37/12348674/7206182a2897/jciinsight-10-175917-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd37/12348674/746077ae28b5/jciinsight-10-175917-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd37/12348674/769facef7021/jciinsight-10-175917-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd37/12348674/263807c67e08/jciinsight-10-175917-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd37/12348674/aea704907454/jciinsight-10-175917-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd37/12348674/7206182a2897/jciinsight-10-175917-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd37/12348674/746077ae28b5/jciinsight-10-175917-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd37/12348674/769facef7021/jciinsight-10-175917-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd37/12348674/263807c67e08/jciinsight-10-175917-g005.jpg

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