文献类型：期刊文献

英文题名：Lipid metabolic regulation of neuroinflammation in Alzheimer's disease

作者：Li, Tingting[1];Guo, Kanglin[2];Ma, Yongxia[1];Zhao, Jianjun[3];Cao, Yanchun[3];Zhang, Run[3];Li, Xiang[1];Wei, Jing[1];Ma, Yufang[1];Zhu, Zongxia[1];Zhao, Dongrong[4]

第一作者：Li, Tingting

通信作者：Zhao, DR[1]

机构：[1]Lanzhou Second Peoples Hosp, Dept Psychiat, Lanzhou, Gansu, Peoples R China;[2]Lanzhou Third Peoples Hosp, Dept Psychiat, Lanzhou, Gansu, Peoples R China;[3]Gansu Univ Chinese Med, Sch Tradit Chinese & Western Med, Lanzhou, Gansu, Peoples R China;[4]Gansu Prov Hosp, Dept Psychiat, Lanzhou, Gansu, Peoples R China

第一机构：Lanzhou Second Peoples Hosp, Dept Psychiat, Lanzhou, Gansu, Peoples R China

通信机构：[1]corresponding author), Gansu Prov Hosp, Dept Psychiat, Lanzhou, Gansu, Peoples R China.

年份：2026

卷号：17

起止页码：1815719

外文期刊名：FRONTIERS IN IMMUNOLOGY

收录：;Scopus(收录号：2-s2.0-105040660021);WOS:【SCI-EXPANDED(收录号:WOS:001773708500001)】；

基金：The author(s) declared that financial support was received for this work and/or its publication. This work was supported by Project of Lanzhou Youth Science and Technology Talent Innovation Project (2024-QN-124). Lanzhou Health and Medical Research Projects (A2024023).

语种：英文

外文关键词：Alzheimer's disease; apolipoprotein E (APOE); fatty acids; gut-brain axis; lipid metabolism; metabolic dysregulation; microglia; neuroinflammation

摘要：Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by beta-amyloid deposition, tau pathology, and sustained neuroinflammation. Increasing evidence indicates that dysregulated lipid metabolism is not merely a metabolic disturbance but a critical modulator of inflammatory responses driving AD pathogenesis. The brain, one of the most lipid-enriched organs, relies on tightly controlled lipid homeostasis to maintain neuronal function and synaptic integrity. Alterations in fatty acid composition, apolipoprotein E (ApoE) isoforms, lipoprotein lipase activity, and lipid-derived signaling mediators profoundly reshape microglial activation states and inflammatory cascades. Obesity, insulin resistance, and gut microbiota dysbiosis further exacerbate systemic and central lipid imbalance, amplifying neuroinflammatory signaling through cytokine networks and blood-brain barrier disruption. Notably, polyunsaturated fatty acids and lipid mediators exert dual immunomodulatory effects, influencing beta-amyloid aggregation, oxidative stress, and microglial polarization. This review synthesizes recent advances in understanding how lipid metabolism modulates neuroinflammation and microglia-neuron crosstalk in AD, highlighting emerging therapeutic strategies targeting lipid-inflammation axes as promising avenues for disease modification.