Parkinson's disease and glucose metabolism impairment

被引:0
|
作者
Chen, Liangjing [1 ,2 ]
Wang, Chunyu [1 ,2 ]
Qin, Lixia [1 ,2 ]
Zhang, Hainan [1 ,2 ]
机构
[1] Cent South Univ, Xiangya Hosp 2, Dept Neurol, Changsha 410011, Peoples R China
[2] Cent South Univ, Xiangya Hosp 2, Clin Med Res Ctr Stroke Prevent & Treatment Hunan, Dept Neurol, Changsha 410011, Peoples R China
来源
TRANSLATIONAL NEURODEGENERATION | 2025年 / 14卷 / 01期
基金
中国国家自然科学基金;
关键词
Parkinson's disease; Glucose metabolism; Mechanisms; Therapeutic drugs; KETOGLUTARATE DEHYDROGENASE COMPLEX; MILD COGNITIVE IMPAIRMENT; K-ATP CHANNELS; ALPHA-SYNUCLEIN; MITOCHONDRIAL COMPLEX; CEREBROSPINAL-FLUID; DIABETES-MELLITUS; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; SUBSTRATE UTILIZATION; DOPAMINERGIC-NEURONS;
D O I
10.1186/s40035-025-00467-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Parkinson's disease (PD) is the second most common neurodegenerative disorder. PD patients exhibit varying degrees of abnormal glucose metabolism throughout disease stages. Abnormal glucose metabolism is closely linked to the PD pathogenesis and progression. Key glucose metabolism processes involved in PD include glucose transport, glycolysis, the tricarboxylic acid cycle, oxidative phosphorylation, the pentose phosphate pathway, and gluconeogenesis. Recent studies suggest that glucose metabolism is a potential therapeutic target for PD. In this review, we explore the connection between PD and abnormal glucose metabolism, focusing on the underlying pathophysiological mechanisms. We also summarize potential therapeutic drugs related to glucose metabolism based on results from current cellular and animal model studies.
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收藏
页数:21
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