Parkinson's disease (PD) is a neurodegenerative disease that is common in middle‐aged and elderly people, and its onset is related to multiple factors, such as heredity, environment, and age. The vesicle protein sorting 35 (VPS35) gene was found to be a late‐onset autosomal dominant familial PD (PARK17) causative gene. The protein encoded by this gene is located in the endosome and aggregates with other membrane proteins to form a retromer complex, which participates in the membrane protein cycle between the endosome and the Golgi network. Increasing evidence shows that VPS35 may participate in the pathogenesis of PD by affecting autophagy, mitochondria, neurosynaptic transmission, dopamine signaling pathways, and so forth, and it can interact with other disease‐causing genes of familial PD. This article aimed to review the functions of VPS35 and the mechanism of its mutations in PD that have been discovered in recent years.

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Mitophagy is a process of removing damaged mitochondria, transferring damaged mitochondria to lysosomes for degradation, thereby regulating the quality of mitochondria and maintaining the stability of the intracellular environment. CME(Clathrin-mediated-endocytosis)plays an important role in the endocytosis and recovery of vesicles. It is also the main way for large parts of substances to enter cells, and it is widely involved in the signal transduction of various physiological activities of cells. Therefore, this study used pentylenetetrazol to ignite the abnormal mitochondrial autophagy in the chronic epilepsy model and the epilepsy model without magnesium-induced neurons. Subsequently, the autophagy inhibitor 3-MA was used to further observe that the inhibition of autophagy caused a decrease in the fluorescence uptake of Tf-A488 in the primary cultured neurons and the hippocampus of experimental mice, and the inhibition of mitochondrial autophagy could inhibit the function of CME. Finally, through PTZ epilepsy model and kainic acid model, we observed the effect of 3-MA on epilepsy behavior and its in-body field potential, and finally clarify the possible mechanism of mitochondrial autophagy regulating CME and participating in epilepsy.

Background Peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), regulated by AMPK, is an important regulator of mitochondrial fusion. At present, whether the AMPK/PGC-1α signaling pathway regulates mitochondrial dynamics in epileptic rats is still unknown. Methods Adult male Sprague-Dawley (SD) rats were randomly divided into five groups: the control group (0.9% saline, n = 5), the EP groups (lithium-pilocarpine was used to induce epilepsy, and tissues were harvested at 6 and 24 h, every time point n = 5), the EP + Compound C group (the specific inhibitor of PGC-1α, 15 mg/kg in 2% DMSO, n = 5), and the EP + DMSO group (0.9% saline + 2% DMSO, n = 5). To observe the seizure susceptibility of the rats to epilepsy by behavioral study. MFN1, MFN2, and PGC-1α were measured using the Western blot and the immunofluorescence analysis. Results In this study, the behavioral results indicate that the seizure susceptibility of the rats to epilepsy was increased when the expression of PGC-1α was inhibited. Subsequently, Western blot results suggested that the expression level of both MFN1 and MFN2 in the hippocampus was higher at 6 and 24 h after an epileptic seizure. Besides, the expression of PGC-1α and MFN2 was significantly decreased in the hippocampus when the epileptic rats were treated with Compound C. Furthermore, the immunofluorescence analysis of the localization of MFN1/2 and PGC-1α showed that MFN1/2 was mainly expressed in neurons but not astrocytes in the hippocampus and cerebral cortex of rats. Meanwhile, PGC-1α colocalized with the excitatory post-synaptic marker PSD95, suggesting that PGC-1α may regulate the seizure susceptibility of the rats by mediating excitatory post-synaptic signaling. Conclusion The AMPK/PGC-1α signaling pathway may play an important role in the lithium-pilocarpine-induced epileptic rat model by mediating the expression of fusion proteins.

The incidence of incomplete partition Type I inner ear malformation is very low; therefore, bacterial meningitis caused by this malformation is also rare. Here, we report a case of such a patient. This case is a young female patient, who is 7 years old, began to have recurrent headaches, and after 5 years, also began to have chest and back pain. The doctor diagnosed meningitis, and the anti‐infection treatment was effective. She was followed up annually and continued to have outbreaks repeatedly for 17 years, but the cause of repeated infection was not found. After a detailed diagnosis and treatment in our hospital, the patient was finally diagnosed with incomplete partition Type I inner ear malformation, resulting in repeated bacterial meningitis. The patient recovered well after surgical treatment, and the symptoms did not recur after 1‐year follow‐up.