Study on the relationship between the risk of Parkinson's disease complicated with cerebral infarction and the serum level of tyrosine hydroxylase and its potential influencing factors / 公共卫生与预防医学

Objective To explore the relationship between serum levels of tyrosine hydroxylase (TH) and the risk of cerebral infarction in Parkinson's patients. Methods A total of 129 patients with confirmed Parkinson's disease who were hospitalized in our hospital were selected, among the 58 patients had Parkinson's disease complicated with cerebral infarction (complicated with cerebral infarction group), and the remaining 71 patients had Parkinson's disease alone (control group). Blood TH levels and other potential related information were collected retrospectively at the time of diagnosis. Comparative analysis of data was performed using SPSS software. Results Comparing the serum TH expression levels in patients with Parkinson's disease and patients with cerebral infarction at admission , the serum TH level in patients with cerebral infarction was lower. Results also showed that the levels of CRP, IL-6, MDA, and Hcy were higher in patients with cerebral infarction, while PON-1 level was lower. In addition, patients with cerebral infarction had lower motor ability (higher UPDRS Ⅲ score). Further regression analysis was carried out with the occurrence of Parkinson's disease complicated with cerebral infarction as the dependent variable and the potential influencing factors as the independent variable. The results indicated that factors such as low expression of TH, high expression of inflammatory factors, and high expression of oxidative stress factors were positively correlated with the risk of complications of the two diseases. Conclusion The low expression of TH, inflammatory state and high oxidative stress state are the potential risk factors for Parkinson's disease complicated with cerebral infarction, which deserves clinical attention.

Long Noncoding RNA NEAT1 Aggravates Aβ-Induced Neuronal Damage by Targeting miR-107 in Alzheimer's Disease

PURPOSE: Alzheimer's disease (AD) is the most common neurodegenerative disease, with a rising prevalence worldwide. Long noncoding RNAs (lncRNAs) have been found to play important roles in the development and treatment of AD. However, the exact role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in neuronal damage in AD is largely unknown. MATERIALS AND METHODS: The AD model was established in SH-SY5Y and SK-N-SH cells via treatment with amyloid β1−42 (Aβ). The expression of NEAT1 and microRNA-107 (miR-107) was measured by quantitative real-time polymerase chain reaction. Cell viability and apoptosis were detected by MTT assay, immunocytochemistry, and flow cytometry. The expression of phosphorylated tau protein (p-Tau) was measured by Western blot. The interaction between NEAT1 and miR-107 was explored by bioinformatics analysis, luciferase activity, and RNA immunoprecipitation assays. RESULTS: NEAT1 expression was enhanced in Aβ-treated SH-SY5Y and SK-N-SH cells, and its knockdown attenuated Aβ-induced inhibition of viability and promotion of apoptosis and p-Tau levels. NEAT1 was indicated as a decoy of miR-107. miR-107 abundance was reduced in Aβ-treated cells, and its overexpression reversed Aβ-induced injury. Moreover, interference of miR-107 abated silencing of NEAT1-mediated inhibition of neuronal damage in Aβ-treated SH-SY5Y and SK-N-SH cells. CONCLUSION: LncRNA NEAT1 aggravated Aβ-induced neuronal damage by sponging miR-107, indicating a novel avenue for treatment of AD.

The effect of low-frequency transcranial magnetic stimulation pretreatment on seizures, the expression of B / 中华物理医学与康复杂志

Objective To study the possible mechanisms by which repetitive transcranial magnetic stimulation (rTMS) pretreatment antagonizes seizures induced by lithium chloride-pilocarpine and any correlation with antiapoptosis in hippocampal CA1 neurons.Methods Thirty rats were randomly divided into a control group, a sham stimulation group and an rTMS pretreatment group. The rTMS pretreatment group was pretreated on 7 consecutive days with low-frequency rTMS (0.5 Hz, 75％ of threshold intensity, 20 times/bundle, and 5 bundles/d), while the sham-stimulation group was sham-stimulated with a similar sound. Lithium chloride-pilocarpine ( LPC ) was used to induce a model epileptic state.Epileptic stroke latency and severity were recorded ; neuronal morphology was observed using hematoxylin and eosin (HE) staining; mean positive-reactive cell number and mean optical density and absorbance of B cell lymphoma/leukemia gene-2 (Bcl-2) were recorded, and Fas and Caspase-3 protein in the hippocampal CA1 region were observed with immunohistochemistry.Results Compared with the sham stimulation group, epileptic latency in the rTMS pretreatment group was significantly longer. Seizures in the rTMS pretreatment group were less severe, and a number of degenerated neurons were observed to be apoptotic. Bcl-2 protein expression increased at each time point, but Fas and Caspase-3 protein expression decreased.Conclusions rTMS pretreatment has an anti-epilepsy effect. The possible neuronal protection might be produced by regulating the expression of Bcl-2, Fas and Caspase-3 protein in the hippocampus.