Role of metabolic dysfunction and inflammation along the liver-brain axis in animal models with obesity-induced neurodegeneration  被引量:1

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作  者:Evridiki Asimakidou Eka Norfaishanty Saipuljumri Chih Hung Lo Jialiu Zeng 

机构地区:[1]Department of Clinical Neurosciences,University of Cambridge,Cambridge,UK [2]School of Applied Science,Republic Polytechnic,Singapore,Singapore [3]Lee Kong Chian School of Medicine,Nanyang Technological University,Singapore,Singapore

出  处:《Neural Regeneration Research》2025年第4期1069-1076,共8页中国神经再生研究(英文版)

基  金:supported by a Presidential Postdoctoral Fellowship (021229-00001) from Nanyang Technological University,Singapore (to JZ);a Lee Kong Chian School of Medicine Dean’s Postdoctoral Fellowship (021207-00001) from NTU Singapore;a Mistletoe Research Fellowship (022522-00001) from the Momental Foundaton,USA (to CHL)

摘  要:The interaction between metabolic dysfunction and inflammation is central to the development of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease.Obesity-related conditions like type 2 diabetes and non-alcoholic fatty liver disease exacerbate this relationship.Peripheral lipid accumulation,particularly in the liver,initiates a cascade of inflammatory processes that extend to the brain,influencing critical metabolic regulatory regions.Ceramide and palmitate,key lipid components,along with lipid transporters lipocalin-2 and apolipoprotein E,contribute to neuroinflammation by disrupting blood–brain barrier integrity and promoting gliosis.Peripheral insulin resistance further exacerbates brain insulin resistance and neuroinflammation.Preclinical interventions targeting peripheral lipid metabolism and insulin signaling pathways have shown promise in reducing neuroinflammation in animal models.However,translating these findings to clinical practice requires further investigation into human subjects.In conclusion,metabolic dysfunction,peripheral inflammation,and insulin resistance are integral to neuroinflammation and neurodegeneration.Understanding these complex mechanisms holds potential for identifying novel therapeutic targets and improving outcomes for neurodegenerative diseases.

关 键 词:Alzheimer’s disease inflammatory cytokines insulin resistance LIPID 

分 类 号:R589[医药卫生—内分泌] R741[医药卫生—内科学] R-332[医药卫生—临床医学]

 

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