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- W4377019977 endingPage "110672" @default.
- W4377019977 startingPage "110672" @default.
- W4377019977 abstract "Impairments in systematic and regional glucose metabolism exist in patients with Parkinson’s disease (PD) at every stage of the disease course, and such impairments are associated with the incidence, progression, and special phenotypes of PD, which affect each physiological process of glucose metabolism including glucose uptake, glycolysis, tricarboxylic acid cycle, oxidative phosphorylation, and pentose phosphate shunt pathway. These impairments may be attributed to various mechanisms, such as insulin resistance, oxidative stress, abnormal glycated modification, blood-brain-barrier dysfunction, and hyperglycemia-induced damages. These mechanisms could subsequently cause excessive methylglyoxal and reactive oxygen species production, neuroinflammation, abnormal aggregation of protein, mitochondrial dysfunction, and decreased dopamine, and finally result in energy supply insufficiency, neurotransmitter dysregulation, aggregation and phosphorylation of α-synuclein, and dopaminergic neuron loss. This review discusses the glucose metabolism impairment in PD and its pathophysiological mechanisms, and briefly summarized the currently-available therapies targeting glucose metabolism impairment in PD, including glucagon-likepeptide-1 (GLP-1) receptor agonists and dual GLP-1/gastric inhibitory peptide receptor agonists, metformin, and thiazoledinediones." @default.
- W4377019977 created "2023-05-19" @default.
- W4377019977 creator A5000486412 @default.
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- W4377019977 creator A5070492082 @default.
- W4377019977 date "2023-07-01" @default.
- W4377019977 modified "2023-10-01" @default.
- W4377019977 title "Glucose metabolism impairment in Parkinson’s disease" @default.
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