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Authors: Ma, Li-Jing | Xu, Ling-Li | Mao, Cheng-jie | Fu, Yun-Ting | Ji, Xiao-Yan | Shen, Yun | Chen, Jing | Yang, Ya-ping | Liu, Chun-Feng

Article Type: Research Article

Abstract: Background: Many optical coherence tomography (OCT) studies have reported alterations in the retinal nerve fiber layer (RNFL) in Parkinson’s disease (PD) and other neurodegenerative diseases. However, whether retinal alterations are a biomarker for PD is still controversial. Objective: To investigate potential correlations between PD and morphological changes in retina using OCT and to determine its usefulness as a biomarker of disease progression in PD. Methods: We performed a cross-sectional study on patients with PD (N = 37) and age-matched controls (N = 42), followed by a longitudinal study of the PD patients (N = 22) over approximately 2.5 years. Results: The average retinal nerve fiber layer …(RNFL) thickness (p  < 0.001), total macular thickness (p  = 0.001), and macular volume (p  = 0.001) were decreased in PD patients compared to controls and had further decreased at the follow-up visit (p  < 0.05 for all). The average RNFL thickness and the total thickness of macular were negatively correlated with age in PD patients at baseline. Linear regression analysis revealed that age (p  = 0.002, p  = 0.003, respectively) and LEDD (p  = 0.011, p  = 0.013, respectively) were correlated to total thickness and volume of macular in 22 PD patients in the follow-up study. However, no correlation was found between RNFL and other parameters. Conclusions: PD progression is associated with pronounced retinal structure changes, which can be quantified by OCT. Patterns of RNFL and macular damage detected by the noninvasive technology of OCT can be a useful biomarker for evaluating the progression of PD. Show more

Keywords: Macular, optical coherence tomography, Parkinson’s disease, retinal nerve fiber layer

DOI: 10.3233/JPD-171184

Citation: Journal of Parkinson's Disease, vol. 8, no. 1, pp. 85-92, 2018

Authors: Ren, Chao | He, Kai-Jie | Hu, Hua | Zhang, Jin-Bao | Dong, Li-Guo | Li, Dan | Chen, Jing | Mao, Cheng-Jie | Wang, Fen | Liu, Chun-Feng

Article Type: Research Article

Abstract: Background: Previous investigations have suggested that decreased expression of glutamate transporter-1 (GLT-1) is involved in glutamate excitotoxicity and contribute to the development of Parkinson’s disease (PD), GLT-1 is decreased in animal models of PD. GLT-1 is mainly expressed in astrocytes, and the striatum is a GLT-1-rich brain area. Objective: The aim was to explore the function and mechanism of astrocytic GLT-1 in PD-like changes. Methods: In the study, PD-like changes and their molecular mechanism in rodents were tested by a behavioral assessment, micro-positron emission tomography/computed tomography (PET/CT), western blotting, immunohistochemical and immunofluorescence staining, and high performance liquid chromatography pre-column derivatization …with O-pthaldialdehida after downregulating astrocytic GLT-1 in vivo and in vitro . Results: In vivo , after 6 weeks of brain stereotactic injection of adeno-associated virus into the striatum, rats in the astrocytic GLT-1 knockdown group showed poorer motor performance, abnormal gait, and depression-like feature; but no olfactory disorders. The results of micro-PET/CT and western blotting indicated that the dopaminergic system was impaired in astrocytic GLT-1 knockdown rats. Similarly, tyrosine hydroxylase (TH) positive immune-staining in neurons of astrocytic GLT-1 knockdown rats showed deficit in cell count. In vitro , knockdown of astrocytic GLT-1 via RNA interference led to morphological injury of TH-positive neurons, which may be related to the abnormal calcium signal induced by glutamate accumulation after GLT-1 knockdown. Furthermore, the GLT-1 agonist ceftriaxone showed a protective effect on TH-positive neuron impairment. Conclusion: The present findings may shed new light in the future prevention and treatment of PD based on blocking glutamate excitotoxicity. Show more

Keywords: GLT-1, astrocyte, Parkinson’s disease, glutamate, calcium signaling

DOI: 10.3233/JPD-212640

Citation: Journal of Parkinson's Disease, vol. 12, no. 1, pp. 295-314, 2022