Dysfunctional Glucose Metabolism in Alzheimer's Disease Onset and Potential Pharmacological Interventions

被引:44
|
作者
Kumar, Vijay [1 ]
Kim, So-Hyeon [2 ]
Bishayee, Kausik [2 ]
机构
[1] Hallym Univ, Coll Med, Inst Cell Differentiat & Aging, Dept Biochem, Chunchon 24252, South Korea
[2] Soonchunhyang Univ, Soonchunhyang Inst Medi Bio Sci, Biomed Sci Core Facil, Cheonan 31151, South Korea
基金
新加坡国家研究基金会;
关键词
Alzheimer's disease; diabetes; glycolysis; ROS; genetic mutation; therapy; NATURAL D-GLUCOSE; OXIDATIVE STRESS; AMYLOID-BETA; A-BETA; NEUROFIBRILLARY TANGLES; INSULIN-RESISTANCE; DIABETES-MELLITUS; MOUSE MODEL; FDG-PET; PROTEIN;
D O I
10.3390/ijms23179540
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alzheimer's disease (AD) is the most common age-related dementia. The alteration in metabolic characteristics determines the prognosis. Patients at risk show reduced glucose uptake in the brain. Additionally, type 2 diabetes mellitus increases the risk of AD with increasing age. Therefore, changes in glucose uptake in the cerebral cortex may predict the histopathological diagnosis of AD. The shifts in glucose uptake and metabolism, insulin resistance, oxidative stress, and abnormal autophagy advance the pathogenesis of AD syndrome. Here, we summarize the role of altered glucose metabolism in type 2 diabetes for AD prognosis. Additionally, we discuss diagnosis and potential pharmacological interventions for glucose metabolism defects in AD to encourage the development of novel therapeutic methods.
引用
收藏
页数:16
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