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Autolysosomal acidification impairment as a mediator for TNFR1 induced neuronal necroptosis in Alzheimer’s disease

Neural Regeneration Research 2024年第9期19卷 1869-1870页

作者： evridiki asimakidou Richard Reynolds Anna M.Barron Chih Hung Lo Department of Clinical Neurosciences University of CambridgeCambridgeUK Department of Brain Sciences Faculty of MedicineImperial College LondonLondonUK Lee Kong Chian School of Medicine Nanyang Technological UniversitySingaporeSingapore

Neuronal necroptosis-an emerging form of regulated cell death associated with neuroinflammatory signaling:Alzheimer’s disease(AD)is characterized by the presence of extracellular amyloid-β(Aβ)plaques and intracellular tau neurofibrillary tangles as well as progressive neuronal loss.Recent evidence has suggested that prolonged neuroinflammation with increased levels of cytokines,arising from neuronal injury,innate immune responses from glial cells,and peripheral inflammation,leads to neuronal death and AD progression.

关键词： Alzheimer death tau Aβ

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

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Neural Regeneration Research 2025年第4期20卷 1069-1076页

作者： evridiki asimakidou Eka Norfaishanty Saipuljumri Chih Hung Lo Jialiu Zeng Department of Clinical Neurosciences University of CambridgeCambridgeUK School of Applied Science Republic PolytechnicSingaporeSingapore Lee Kong Chian School of Medicine Nanyang Technological UniversitySingaporeSingapore

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

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