Abstract
Parkinson’s disease (PD) is a common neurodegenerative disease in middle-aged and elderly individuals. At present, no effective drug has been developed to treat PD. Although a variety of drugs exist for the symptomatic treatment of PD, they all have strong side effects. Most studies on PD mainly focus on dopaminergic neurons. This review highlights the function of glutamic acid transporters (GLTs), including excitatory amino acid transporters (EAATs) and vesicular glutamate transporters (VGLUTs), during the development of PD. In addition, using bioinformatics, we compared the expression of different types of glutamate transporter genes in the cingulate gyrus of PD patients and healthy controls. More importantly, we suggest that the functional roles of glutamate transporters may prove beneficial in the treatment of PD. In summary, VGLUTs and EAATs may be potential targets in the treatment of PD. VGLUTs and EAATs can be used as clinical drug targets to achieve better efficacy. Through this review article, we hope to enable future researchers to improve the condition of PD patients.
Highlights
Parkinson’s disease (PD) is a common neurodegenerative disease characterized by resting tremor, bradykinesia, rigidity, and postural instability
These data indicate that PD can lead to functional changes in astrocytes, which in turn lead to increased extracellular Glu through downregulation of the Glu transporter EAAT1, thereby damaging dopaminergic neurons and causing neurotoxicity
Most studies have found that VGLUT3 plays a crucial role in levodopa-induced dyskinesia, which occurs in patients with PD who have been treated with levodopa over a long period of time
Summary
Parkinson’s disease (PD) is a common neurodegenerative disease characterized by resting tremor, bradykinesia, rigidity, and postural instability. In the acute MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model and 6-hydroxydopamine (6-OHDA)-lesioned rat model of PD, decreased immunoreactivity and gene expression levels of EAAT1 are observed in the striatum (Holmer et al, 2005; El Arfani et al, 2015) Taken together, these data indicate that PD can lead to functional changes in astrocytes, which in turn lead to increased extracellular Glu through downregulation of the Glu transporter EAAT1, thereby damaging dopaminergic neurons and causing neurotoxicity. A series of studies has suggested that the reduced expression levels of VGLUT2 in the STN of mice cause degeneration of midbrain DA neurons (Schweizer et al, 2014, 2016; Moore et al, 2020). Most studies have found that VGLUT3 plays a crucial role in levodopa-induced dyskinesia, which occurs in patients with PD who have been treated with levodopa over a long period of time
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