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作 者:Chia-Wei Huang Nicholas C.Rust Hsueh-Fu Wu Gerald W.Hart
机构地区:[1]Complex Carbohydrate Research Center,University of Georgia,Athens,GA,USA [2]Department of Biochemistry and Molecular Biology,University of Georgia,Athens,GA,USA [3]Center for Molecular Medicine,University of Georgia,Athens,GA,USA
出 处:《Neural Regeneration Research》2023年第4期779-783,共5页中国神经再生研究(英文版)
基 金:supported by the Georgia Research Alliance and the University of Georgia(to GWH)。
摘 要:Alzheimer’s disease is a neurodegenerative disease that affected over 6.5 million people in the United States in 2021,with this number expected to double in the next 40 years without any sort of treatment.Due to its heterogeneity and complexity,the etiology of Alzheimer’s disease,especially sporadic Alzheimer’s disease,remains largely unclear.Compelling evidence suggests that brain glucose hypometabolism,preceding Alzheimer’s disease hallmarks,is involved in the pathogenesis of Alzheimer’s disease.Herein,we discuss the potential causes of reduced glucose uptake and the mechanisms underlying glucose hypometabolism and Alzheimer’s disease pathology.Specifically,decreased O-Glc NAcylation levels by glucose deficiency alter mitochondrial functions and together contribute to Alzheimer’s disease pathogenesis.One major problem with Alzheimer’s disease research is that the disease progresses for several years before the onset of any symptoms,suggesting the critical need for appropriate models to study the molecular changes in the early phase of Alzheimer’s disease progression.Therefore,this review also discusses current available sporadic Alzheimer’s disease models induced by metabolic abnormalities and provides novel directions for establishing a human neuronal sporadic Alzheimer’s disease model that better represents human sporadic Alzheimer’s disease as a metabolic disease.
关 键 词:Alzheimer’s disease amyloid beta BRAIN glucose deficiency glucose uptake HYPOMETABOLISM mitochondrial dysfunction neurodegenerative disease neurons O-GlcNAc Tau
分 类 号:R749.16[医药卫生—神经病学与精神病学]
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