Role of metabolic dysfunction and inflammation along the liver-brain axis in animal models with obesity-induced neurodegeneration
Evridiki Asimakidou1
Eka Norfaishanty Saipuljumri2
Chih Hung Lo3
Jialiu Zeng3
1.Department of Clinical Neurosciences,University of Cambridge,Cambridge,UK2.School of Applied Science,Republic Polytechnic,Singapore,Singapore;Lee Kong Chian School of Medicine,Nanyang Technological University,Singapore,Singapore3.Lee Kong Chian School of Medicine,Nanyang Technological University,Singapore,Singapore
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.
机标关键词：metabolicneurodmodelsaxisrolewithalonganimal
论文发表日期：2025-04-27
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：8( 1069-1076 )
英文信息