Introduction. This study investigated the influence of lockdown during the 2019 coronavirus disease (COVID-19) pandemic on the quality of life of patients with Parkinson’s disease (PD). Methods. We conducted a questionnaire survey involving 113 patients with PD from Xihu District, Hangzhou, Zhejiang. During the epidemic prevention and control period (February 1 to March 31, 2020), patients enrolled were asked to fill out questionnaires, including the “COVID-19 Questionnaire for PD Patients during the Period of Epidemic Prevention and Control” and “39-item Parkinson’s Disease Questionnaire (PDQ-39).” During the phase of gradual release of epidemic prevention and control (April 1 to April 30, 2020), all patients were followed up again, and PDQ-39 questionnaires were completed. Results. The quality of life for patients during the period of epidemic prevention and control was worse than that after epidemic prevention and control (P < 0.001). The biggest problem that they faced was that they could not receive their doctor’s advice or guidance regularly. The quality of life of patients who had difficulty getting doctors’ guidance or those who changed their routine medication due to lockdown was even worse. Telemedicine was quite effective and efficient for patients to get doctors’ guidance during lockdown. Conclusions. The inconvenient treatment during the pandemic directly caused the aggravation of patients’ symptoms and the decline in their quality of life. It is suggested that social media (such as WeChat or Tencent QQ) are used for regular interactions and follow-up appointments for patients with inconvenient medical treatment.

Background: Parkinson's disease (PD) is a common central nervous system degenerative disease in middleaged and elderly people. Our study aimed to illuminate the relationship and mechanism of long-chain noncoding RNA SNHG1 and miRNA (miR)-216a-3p in PD.Methods: Human neuroblastoma cell lines were treated with MPP + to construct a PD model. Realtime fluorescent quantitative PCR was used to detect the cellular expression of SNHG1. Neuronal cell activity and apoptosis were compared before and after SNHG1 knock-down, as was neuronal miR-216a-3p expression. Further, a luciferase reporter gene experiment was performed to verify BAX as the target of miR-216a-3p. Anti-miR-216a-3p and BAX were co-transfected into PD model cells, and neuronal cellular activity and apoptosis were observed. Finally, the potential regulatory network of SNHG1/miR-216a-3p/BAX in PD was investigated. Results:The expression of miR-216a-3p was decreased in the PD model cells, and re-expression reversed the high apoptotic rate and cell vitality inhibition in PD model cells. SNHG1 interacted with miR-216a-3p and negatively regulated its upstream molecules, while miR-216a-3p attenuated the effect of SNHG1 knockdown on neurons. The overexpression of BAX in the PD cell model blocked the damage by miR-216a-3p to neurons. At the same time, SNHG1 acted as a coordinator, mediating the regulation of BAX via miR-216a-3p, thereby affecting the activity and apoptotic rate of neurons in the PD model. Conclusions: SNHG1 interacts with miR-216a-3p to regulate the expression of BAX. This SNHG1/miR-216a-3p/BAX molecular regulatory network is implicated in the pathogenesis of PD.

Objectives: Freezing of gait (FOG) is generally considered as an independent symptom of Parkinson's disease (PD) with a complex pathophysiology. There is a wide range of associated clinical features of FOG reported from different studies without consistent conclusion. Thus, a multicenter, cross-sectional study was designed to investigate the prevalence and clinical features of FOG together with its unique contribution quality of life in Chinese PD patients.Methods: Eight hundred and thirty eight PD patients were consecutively recruited into this study from 12 hospital centers in six provinces in China. Clinical information, including motor and neuropsychological features as well as pharmacological details, was collected.Results: Of 827 PD patients, 245 (29.63%) reported FOG. The prevalence of FOG was strongly correlated with modified H-Y stages and symptomatic duration (p &lt; 0.01). 84.90% freezers experienced FOG during turning and 88.98% experienced when initiating the first step. Compared with non-freezers, freezers reported longer disease duration (7.73 ± 5.44 vs. 4.69 ± 3.94, p &lt; 0.000), higher frequent PIGD phenotype (61.22 vs. 35.91%, p &lt; 0.000), higher scores of UPDRS III (32.85 ± 15.47 vs. 22.38 ± 12.89, p &lt; 0.000), HAMA (10.99 ± 7.41 vs. 7.59 ± 6.47, p &lt; 0.000), HAMD (15.29 ± 10.29 vs. 10.58 ± 8.97, p &lt; 0.000) and lower MMSE score (25.12 ± 5.27 vs. 26.63 ± 3.97, p &lt; 0.000), and higher daily levodopa dosage (432.65 ± 264.31 vs. 319.19 ± 229.15, p &lt; 0.000) with less frequent initial use of dopaminergic agonist (8.57 vs. 14.78%, p &lt; 0.05). Using binary logistic regression, the associated factors of FOG might be non-tremor dominant onset (OR = 3.817, p &lt; 0.000), the presence of anxiety (OR = 2.048, p &lt; 0.000) and imbalance (OR = 4.320, p = 0.012). Freezers had poorer quality of life than non-freezers and FOG impacted PDQ-8 independently.Conclusion: Nearly one third of the PD patients experienced FOG. Its frequency increased with PD progression and FOG reduced independently the quality of life. Non-tremor dominant, disease progression, and anxiety were risk factors of FOG.

Objective. To investigate the potential role of Momordica charantia polysaccharides (MCPs) in Parkinson’s disease (PD) and reveal the molecular mechanism of its function. Method. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (1-methyl-4-phenylpyridinium, MPP+) were used to establish PD mice and cell models. The mice and cells were divided into 4 groups: Control group, Control+MCPs group, PD group, and PD+MCPs group. Pole climbing experiment and Rotarod experiment were used to observe the coordination ability of mice. High-performance liquid chromatography and enzyme-linked immunosorbent assay (ELISA) were used to determine neurotransmitters and metabolites, inflammatory factors TNF-α and IL-1β, oxidative stress-related markers SOD, MDA, and GSH in striatum tissues. Western blot was used to determine the protein levels of tyrosine hydroxylase (TH), oxidative stress-related protein Cytochrome C (Cytochrome C), and apoptosis-related proteins Bcl-2, Bax, and cleaved Caspase-3 in tissues and cells. Moreover, flow cytometry, PI staining, and fluorescence were used to observe cell apoptosis. Finally, the activation effect of MCPs on TLR4/MyD88/NF-κB signaling pathway was observed and verified. Results. Compared with the Control group, MPTP treatment can induce brain damage in mice (all P < 0.05 ), change the metabolic state of neurotransmitters (all P < 0.05 ), induce inflammation (all P < 0.05 ), and induce apoptosis and the occurrence of oxidation reaction (all P < 0.05 ); however, MCPs treatment can significantly reverse the above changes (all P < 0.05 ). In cell models, studies have found that MCPs can play a protective role by regulating the activation state of TLR4/MyD88/NF-κB pathway. Conclusion. This study found that the application of MCPs therapy can play anti-inflammatory, antioxidative stress, and antiapoptotic effects in PD by regulating the activation of the TLR4/MyD88/NF-κB pathway.